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

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. 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. Strep. weeping local infxn Primarily in children Pathogen: Group A strep (B-hemolytic) and Staph Spread = direct contact ERYSIPELAS Group A Strep Common type: Pustules.BACTERIAL INFECTIONS Impetigo Superficial. LFTs. lack of classical tissue inflammatory signs. Sedentary lifestyle Abscess at natal cleft tender. raised. extremes of age. 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. failing previous tx or have scarring Isoretinoin (Accutane) y Teratogen!! y Associated w/ depression y *Monthly blood tests (B-hcg. or muscle in addition to skin Common pathogen: Staph or group A strep. warm and indurated *May develop into perianal fistulas . 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. rapid burrowing through fascial planes. urticaria. fluctuant. severe pain.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. and Gram Bacteria. comorbid conditions. aureus  Can evolve into SSSS Pts have hx of trauma or pharyngitis Small red patch on cheek Turns into painful. drained. TGs) Clinical r/o perirectal and anal abscess Incision + Drainage hot tub folliculitis Tiny pustule. and necrotizine fasciitis Oral antibiotics 7-10 days Systemic toxicity. 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. gas production. local infxn involving CT. Men > women Risk: deep/hairy natal clefts. putrid discharge. back. 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. hot. intravascular volume loss Folliculitis Inflammation of hair follicle Pathogen: Staph. primarily nodulocystic. gloved fingers can easily pass btw two layers to reveal yellow-green necrotic fascia Most important signs: tissue necrosis. occasionally yeast (Candida. honey-colored crusts on erythematous base. erythromycin **Severe acne or moderate acne. Face Bullous type: Acral. contact dermatitis. osteomyelitis. Obesity. DM. tender skin Fever + chills common Regional lymphadenopathy Clinical Wound culture (may help aid + sensitivities) Blood cx (when bacteremia suspected) R/o abscess. Pityrosporum ovale) *Pseudemonas aeruginosa Mechanical (ingrown hairs) risk: Diabetes. cholesterol. Large stable blisters  Almost always caused by S. subq tissue. bullae. shiny red plaque Scarlet fever S. swollen. 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).

genitals Exam: track seen. 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. scaly skin on soles  Assymmetric involvement of hands typical Tinea crurus ( jock itch ): chronic infxn of groin (spares scrotum) Tinea capitis ( ringworm ): diffuse. nails. or blistered w/ pus Gas:  At site of recent injury/surgery  Swelling around injury. excoriated papules Mite may be identifiable by scraping intact tunnels and looking under microscope Severe pruritis. erythematous macules that converge. and shriveled  Risk: Diabetes. secondary bacterial infection of excoriations Classroom epidemics common Body lice: inadequate hygiene. cold. erythematous.FUNGAL INFECTION Tinea versicolor Infection w/ Malassezia furfur (normal skin yeast) Risk: Humid and sweaty conditions. scaly patches of varying color Pale. crowded living conditions Seen on hair follicles or clothing Head lice:  OTC pyrethrin (RID) + mechanical removal of nits Body lice:  Wash body. atherosclerosis Wet: baterial infxn w/ skin flora Gas: clostridium perfringens infxn Heel + tips of toes Very PAINFUL Underside of foot + toes At pressure points. smoking Wet:  tissue appears bruised. and hair) Organisms: Microsporum. lack mobility. fat. 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. PAINLESS Dry:  Early: dull ache. swollen. so provide symptomatic tx Intense pruritis. 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. perfringens)  Susceptible pts should maintain careful foot care and avoid trauma . change in pigmentation takes months to return to normal Candidasis Clinical KOH prep: hyphae + pseudospores Oral: Oral fluconazole. oily skin. Nystatin swish and swallow Skin: Topical antifungals. velvety pink or whitish. dry. skin turns pale then dark red  Bacteria rapidly destructive of tissue gas separates Clinical Surgical debridement. 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). cannot easily be scraped off Risk: antibiotics. steroids. 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. Epidermophyton Risk: Pets. keep skin clean and dry PARASITIC Lice Live off blood Head louse: scalp. clothes. chronic maceration of skin (athetic activities) Tinea corporis: scaly. immune compromise. diabetes Skin: pink. especially at night + after hot showers MC sites: hands. circular. Cushings syndrome. diabetes. Burrowing pruritis intensity when allergy develops Spread: close contact Hx of pruritis in several family members Pruritis may persist 2 weeks after tx. and pallor of flesh  w/ necrosis (usually toe) becomes bluish-black. layes eggs as nits attached to hair Body louse: clothing. vasculopathy. axillae. pruritic eruption w/ sharp. 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. Immunosuppression Chest and back Small. 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. hypopigmented macules or hyperpigmented (thickened scale)  Do not tan and are NOT scaly  Scale on scraping Oral: painless white plaques. Trichophyton. peripheral circulation.

chocolate. telangiectasia. topical antipruritics. DM. Persistent  Penile. lightened in tinea versicolor) Topical/systemic psoralens Exposure to sunlight or PUVA Must wear sunscreen (depigmented skin lacks protection) . sharply demarcated. polygonal papules Wickmans striae (white stripes). esp. spicy foods. acne) Environmental triggers (infectious agents. piebaldism. Polygonal. genitalia Peri-orificial lesions or lesions on finger tips Total depigmentation (vs. hot drinks. thicker scale)  Drug eruptions Clinical Histo: total absence of melanocytes r/o: postinflammatory hypopigmentation. papules. abnormal flushing response to various substances Do NOT have comedones (vs. symmetric papules w/ fine cigarette paper scale. face.healthy tissue predisposes to infxn  MEDICAL EMERGENCY! MISCELLANEOUS SKIN DISORDERS Acanthosis nigrans Sin in intertriginous zones (genital and axillary regions. 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. 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. depigmented macules/patches on otherwise normal skin  Hands. 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. 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. C P disease:  Planar. and pustules Women.  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. sunlight. Fasting glucose to r/o insulin resistance Topical retinoids but typically not treated Encourage to lose weight!! Avoid triggers that aggravate vasodilation (coffee. tea. middle-aged 30-50. pernicious anemia Pts w/ malignant melanoma may develop antimelanocyte immune response vitiligo Small. Oral have more chronic course. Purple  Pruritis. systemic antihistamines Severe: short course of systemic steroids Vitiligo Disease of depigmentation Chronic + Progressive Serologic markers of autoimmune dz  Anithyroid Abs. can be induced by drugs. 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. localized erythema. Koebner s phenomenon Rosacea Chronic inflammatory condition w/ facial flushing. associated w/ Hep. Perioral. scleroderma.

in childhood + w/ intermittent exposure)  Congenital melanocytic nevi. papules. or PUVA Stage II: Systemic retinoids. scaly papules w/ erythematous base  Sandpaper-like texture Face.  # of nevi. interferon. or chemo Photopheresis = mainstay of tx More extensive/advanced: Radiation therapy . liver. retinoids. + patches <10% BSA w/ NO nodes Stage II: limited or generalized skin involvement + palpable LNs or u1 skin tumors w/ multicentric. pruritic Stage 1: limited plaques. HHV-8. Pathogenesis: Chronic immunostimulation helper T cells to gather in epidermis Risk: Industrial exposure to irritation chemicals Chronic. Not a fungus. However. 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.  Dysplastic nevi. surveillance essential Palliative Kaposi s Sarcoma (KS) Vascular proliferative dz attributed to herpesvirus. lower lip. deep cryotherapy. monoclonal antibodies. forearms. 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. basaloid epidermal cells w/ horn pseudocysts (prominent follicular openings) r/o actinic keratosis. hand dorsum. intense bursts of sun exposure (esp. bald scalp. SCC. 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. ulceration. locally destructive. 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. internal organs can be involved (LNs. ears nd MC = back and chest >50 years Exophytic. More common in men Early lesion: nonspiecific. or axillae) Clinical diagnosis Histo: hyperplasia of benign. other sun-exposed areas Excision. 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. superficial radiation therapy. and Mohs surgery Cure rates >95% Melanoma MC life-threatening dermatologic dz Risk:  Short. 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. stuck on appearing papules/plaques May become irritated spontaneously or by external trauma (esp. curettage and electrodesiccation/cautery. waxy brown. progressive neoplastic proliferation of T cells. chemo. topical 5-FU. in groin. lentigo (focal in melanocytes). 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. 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. psoriatic-appearing plaque palpable. breast. almost in all pts >40 When may erupt suddenly.DYSPLASIAS Seborrheic keratosis Benign thickening s of epidermis Very common.  Immunosuppression Genetics: Familial atypical mole. 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. 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.

+ lymphadenopathy Lupus erytehmatosus (discoid. central clearing ( bulls eye ) Secondary (early disseminated):  Migratory polyarthropathy  Neurologic phenomena (bells palsy)  Meningitis  Myocarditis rd  Conduction abnormalities (3 deg. drugs.Sezary s syndrome: leukemic phase of CTCL circulating Sezary cells in peripheral blood. 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. subacute. MR. weight loss. casts) A ANA + (highly sensitive. and cardiovascular systemis Risk:  Female  Age 35-50 Raynauds. ash-leaf hypopigmented macules NO abd pain + red urine Vesicles on back of hand after drinking alcohol. 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. sebaceous adeomas. waxy papules on face Primary systemic (AL) and Seconary systemic (AA): Kidneys. dysphagia. GI. Leukopenia. myalgias. C Retinal phacomas.Oral ulcers P Photosensitivity A Arthritis M Malar rash I Immunologic criteria N Neuro sx (Lupus cerebritis. seizures. and/or arthralgias Primary (early-localized):  Erythema migrans (small erythematous macule/papule at tick-biting site expands slowly weeks-days)  Border macular or raised. heart. 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. pulmonary. 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. 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. mask-like face. anorexia. malaise. GU. seizures) E Elevated ESR R Renal dz (proteinuria. not specific) S Serositis (pleural or pericardial effusion) H Hematologic abnormalities (Anemia. fatigue. headache. renal. 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 . symmetric joint pain *Have 4 criteria D Discoid rash O . erythroderma. 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.

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