• ROS, PMH, h/o skin lesions, travel, exposures (pets or hobbies), sick contacts, immunizations, sexual hx, menstrual hx, new medication hx (including OTC)
• Physical exam: Assess for fever, hypotension, tachycardia, AMS; Nikolsky sign?
• Distribution of rash: Central/peripheral, flexor/extensor surface, dermatomal, intertriginous, follicular, acral, localized/grouped/regional/generalized, sun-exposed, mucosal
• Shape or configuration: Annular (ring-shaped), round/nummular/discoid (coin-shaped), targetoid, arcuate (arc-shaped), linear, serpiginous, reticular (net-like/lacey), whorled (marble-like), polycyclic (coalescing circular/ring-shaped lesions)
• Characterize rash based on morphology (see table)
VIRAL EXANTHEMS
Measles (Rubeola; “First Disease”)
Definition
• Highly contagious dz caused by the measles virus, spread by droplet contact
• Failure rate of vaccine estimated to be <0.2%; typically seen in nonimmunized
History
• Assess vaccination status, as this guides serologic interpretation
• Typically occurs in winter & spring months. Incubation period of 8–12 d.
• Viral prodrome (fever, cough, coryza, conjunctivitis, but also HA, photophobia, sore throat not uncommon), lasting 3 d, typically 3rd decade of life
Physical Findings
• Fever; adenopathy
• Koplik spots: Small, irregular spots on buccal mucosa w/ bluish coloration during prodromal period (pathognomonic); usually fades w/i 3 d of rash
• Rash starts behind ears, on the face, & neck beginning as discrete purple-red maculopapular lesions & patches. Over 2–3 d spreads to trunk/extremities & becomes confluent; rash may extend to palms; typically lasts 3–7 d & fades.
Diagnostics
• Routine labs rarely indicated, but CBC may show leukopenia
• Lab confirmation: Measles serologies (enzyme immunoassay for measles IgG & IgM), throat or nasopharyngeal swab for viral isolation/RT-PCR. Contact lab specialist.
Treatment
• Supportive, treat cx (see below)
Disposition
• Home if absence if cx
• ID consultation should be considered
• Measles is designated as notifiable infectious dz at national level by CDC; requires notification w/i 24 h
Pearl
• Highly contagious, thus contacts should be aware
• Milder forms can occur in children & adults w/ partial immunity
• Cx: OM (most common), pneumonia (most common severe complication) mastoiditis, croup, febrile szs, postinfectious encephalitis, keratitis, corneal ulcerations, blindness, TTP, myocarditis, pericarditis, myositis
Rubella (German Measles; Three-day Measles; “Third Disease”)
Definition
• Dz of childhood caused by rubella virus, spread by droplet contact
• Causes 2 distinct syndromes: A mild self-limited postnatal infection occurring in early childhood as well as a severe, disseminated congenital infection (represents the “R” in “TORCH” congenital infections). Only postnatal infection will be discussed.
History
• Assess vaccination status
• Typically occurs in winter & spring months. Incubation period of 2–3 wk.
• Viral prodrome (malaise cough, sore throat, low-grade fever, HA); arthralgias also common
Physical Findings
• Low-grade fever, suboccipital & posterior auricular/cervical adenopathy may be present
• Pink maculopapular rash that begin on face/forehead w/ caudal progression to trunk/extremities, may coalesce; typically lasts 3 d & fades
Diagnostics
• Routine labs rarely indicated, but CBC may show leukopenia &/or TCP
• Lab confirmation: Rubella serologies (enzyme immunoassay, latex agglutination, IFA), throat or nasopharyngeal swab for viral isolation/RT-PCR. Contact lab specialist.
Treatment
• Supportive, treat cx (encephalitis, arthritis, TCP)
• Avoid contact w/ pregnant women (severe congenital defects)
Disposition
• Home
• Rubella is designated as notifiable infectious dz at national level by CDC; requires notification w/i 24 h
Erythema Infectiosum (“Fifth Disease”)
Definition
• Viral exanthem caused by Parvovirus B19
• Spread by respiratory droplets & secondary infectious rates by household contacts are high. Transmission via blood products has also been described.
History
• Affects mainly school-age children (2–14 y/o) in late winter/spring months
• Incubation period of 1–2 wk w/ a prodrome of low-grade fever, malaise, HA
• Arthropathy is a common manifestation in adults w/ arthralgias or inflammatory arthritis
Physical Findings
• Intensely red face (“slapped cheek”) w/ circumoral pallor lasting 1–4 d followed by a generalized rash that has a reticular/lacey pattern, particularly on extensor surfaces of the extremities w/ progression to trunk/buttocks/thighs; spares palms & soles; can wax & wane for weeks
Diagnostics
• Routine labs rarely indicated; consider CBC, reticulocyte count, & haptoglobin in pts w/ known hemolytic anemia (ie, hereditary spherocytosis) or hemoglobinopathies (ie, SCD)
• Lab confirmation: Serologic testing, DNA assays (direct hybridization)
Treatment
• Symptomatic
• If complicated (see below), can consider course of IVIG in consultation w/ hematology
Disposition
• Home
Pearl
• Cx: Arthritis (most common), transient aplastic crisis (pts w/ hemolytic anemias & hemoglobinopathies [ie, SCD]), persistent anemia (pure red cell aplasia), fetal hydrops & spontaneous miscarriage
Roseola Infantum (Exanthema Subitum; “Sixth Disease”)
Definition
• Dz of children 3–36 mo (95%) caused by HHV-6 & HHV-7
• It is the most common exanthema in children <3 y/o
• Mechanism of transmission unclear, but presumed to be via salivary secretions
• 3 basic stages of infection: Acute infection in infants/young children, latent infection in adults w/ possible excretion in saliva, & reactivation/reinfection, particularly in immunocompromised
• Although rare, primary infection in adulthood may cause a heterophile-negative mononucleosis-like illness
History
• No seasonal variation is observed & incubation period is 1–2 wk
• High fevers, occasional febrile sz, rash begins after defervescence
• May have prodromal coryza, HA, & periorbital edema
Physical Findings
• Despite fever, pts are nontoxic appearing; lymphadenopathy is common
• Pink macules 2–3 mm, start on trunk & spreads to extremities, clears in 1–2 d
Diagnostics
• Routine labs rarely indicated, but CBC may show leukopenia
• Primary infection w/ HHV-6 is difficult to confirm diagnostically
Treatment
• Supportive
• Complicated dz in immunosuppressed pts (see below) may be treated w/ ganciclovir or foscarnet
Disposition
• Home
Pearls
• Most common complication is febrile szs
• Cx: Reactivation in adults & immunocompromised pts may be a/w encephalitis as well as bone marrow suppression (particularly in transplant recipients) leading to pneumonitis, hepatitis, transplant failure or GVHD
Herpes Simplex 1 and 2 (HHV-1 and HHV-2)
Definition
• HSV-1 mainly implicated in orofacial lesions & HSV-2 in genital infections; however, crossover secondary to sexual practices & autoinnoculation can occur
• Primary herpetic gingivostomatitis: Result of initial exposure to HSV-1; virus then migrates to trigeminal ganglion via sensory nerve; viral reactivation can occur in >1/3 pts
• Herpes labialis/recurrent intraoral herpes (cold sore, fever blister): Affects perioral skin & mucous membranes, respectively; represents reactivation w/ local replication
• Herpes genitalis: Transmitted via sexual contact w/ infected partner. Subclinical viral shedding is common thus infected pts may not report contact w/ active lesions. Lesions appear on genitals & mucous membranes of genitalia as well as perineum, thighs or perianal area.
• Both forms of HSV are highly transmissible through contact w/ active lesions, respiratory droplets, contaminated inanimate objects (ie, sharing kitchen/bathroom utensils for HSV-1) & infected exudates/secretions
• Reactivation can be triggered by fever, menstruation, sun exposure, URI, stress (physiologic/emotional), immunosuppression, etc. Most often recurrences spontaneous.
History
• Herpes gingivostomatitis: Usually affects young children, prodromal fever, malaise, dysphagia, lymphadenopathy followed by oral/perioral vesicles, oral ulcers, & gingivitis lasting 1–2 wk
• Herpes labialis: Prodromal pruritus, tingling, burning followed by rash typically at mucocutaneous junction at lips lasting 1–2 wk; sore throat & lymphadenitis common
• Herpes genitalis: Prodrome of localized pain, tingling or burning in genital region. Pts may also have constitutional sx w/ HA, fever, inguinal adenopathy, malaise → rash. Can be primary or recurrent. Primary lesions last 2–6 wk & clinically worse. Primary infection usually begins 6 d after sexual contact; median 4 recurrences/y.
• RF for genital herpes: Number of lifetime sex partners, multiple partners, h/o STI, HIV
Physical Findings
• Herpes genitalis/labialis: Grouped vesicles on erythematous base (“dewdrop on a rose petal”) → crusted lesions
• Recurrent intraoral herpes: Unilateral crop of small vesicles → small round vesicles on palate & gingiva. May be confused w/ aphthous stomatitis.
Diagnostics
• Tzanck smear, viral cultures, PCR, biopsy available but are rarely needed
Treatment
• Pain control, hydration
• Herpes labialis: Topical therapy (docosanol 10% cream, penciclovir 1% cream, acyclovir 5% ointment, cidofovir 0.3 or 1% gel) & oral therapy (Acyclovir, Famciclovir, Valacyclovir) may decrease sxs & time to healing; sunscreen may decrease relapses.
• Herpes genitalis: Therapy differs for primary infection, recurrence & suppressive therapy
• Acyclovir 400 mg TID for 7–10 d (primary) or 5 d (recurrent)
• Famciclovir 250 mg TID for 7–10 d (primary) or 125 mg BID for 5 d (recurrent)
• Valacyclovir 1 g BID for 7–10 d (primary) or 1 g daily for 5 d (recurrent)
• IV acyclovir 5–10 mg/kg q8h should be given for severe or disseminated dz
Disposition
• Home
Pearls
• Cx: Encephalitis, hepatitis, pneumonitis
• Pts should be counseled on safe sex practices & prevention of spreading dz
Guideline: Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines, 2010. MMWR Morb Mortal Wkly Rep. 2010;59:1–110.
Varicella (“Chickenpox,” HHV-3)
Definition
• Highly contagious caused by primary infection w/ VZV. Varicella attack rates among susceptible household contacts exposed to VZV are ∼90%; more limited exposure result in transmission rates 10–35%.
• Common childhood illness a/w fever & generalized pruritic vesicular rash
• Affects children usually b/w 5 & 10 y/o
• Can cause disseminated infection (see Herpes Zoster)
• Transmitted via respiratory droplets or vesicular fluid from infected person. Virus then inoculated at mucous membranes → spread to regional LNs →1° viremia w/ replication in liver & spleen → 2° viremia w/ mononuclear cell transport to skin & mucous membranes.
History
• Peaks late winter/spring & incubation period about 14 d (range 10–21 d)
• Viral prodromal sxs (fever, malaise, HA, abdominal pain) usually lasting 24–48 h before skin lesions. Rash & new lesion formation over 1–7-d period.
• RFs include household or other personal close contacts (ie, classmate)
Physical Findings
• Maculopapular → vesicular (“dewdrop on a rose petal”) → crusted lesions, often involves the scalp, face, or trunk & may generalize. Rash is pruritic.
• Ulcerative, painful lesions may appear on mucous membranes
Diagnostics
• Routine labs rarely indicated, but CBC may show lymphopenia & transaminitis
Treatment
• Healthy children: Symptomatic/supportive (calamine lotion, colloidal oatmeal baths), avoid salicylates (a/w Reye syndrome in children)
• Oral antiviral therapy should be considered for certain groups at high risk for moderate to severe varicella (healthy persons >12 y/o, those w/ chronic cutaneous or pulmonary disorders, on long-term salicylate therapy, those on short or aerosolized courses of corticosteroids, & pregnant women w/ serious viral-mediated cx)
• IV antiviral therapy prevents progressive varicella & visceral dissemination in high-risk groups. Indicated for those w/ malignancy, bone marrow or organ-transplant recipients, high-dose corticosteroid therapy, congenital T-cell immunodeficiencies, HIV, neonatal varicella, & complicated or disseminated varicella (see below).
Postexposure Prophylaxis
• Antivirals not recommended for prophylaxis
• Varicella vaccine (live attenuated) recommended for exposures in those eligible for vaccine & who do not have e/o immunity, ideally w/i 3–5 d after exposure
• Varicella zoster immune globulin can prevent varicella from developing or lessen severity in high-risk groups & should be given w/i 96 h after exposure in those not eligible for vaccine (allergy, altered immunity, pregnancy, infants)
Preventing Nosocomial Spread
• Pts should be placed on airborne precautions (negative air-flow rooms) & contact precautions until lesions crusted
• Pts should be managed only by providers w/ e/o immunity
• Pregnant ED staff w/o known e/o immunity should avoid contact
Disposition
• Home for uncomplicated cases
• Admission for high-risk groups or those who develop complicated VZV
Pearls
• More severe in adults than children
• Complication in o/w healthy children include bacterial superinfection of skin, transient hepatitis, varicella pneumonia, encephalitis, cerebellar ataxia, myelitis TCP, purpura fulminans, nephritis, arthritis, myocarditis, pericarditis, pancreatitis, etc.
• Can be disseminated in immunocompromised w/ higher risk of cx
• In rare cases, maternal varicella in early gestation can result in a congenital varicella syndrome (microcephaly, mental retardation limb hypoplasias, cutaneous defects, etc.); later in pregnancy, varicella can cause preterm delivery & neonatal varicella
Herpes Zoster (“Shingles,” HHV-3)
Definitions
• Reactivation of VZV in sensory ganglia
• Herpes zoster ophthalmicus: Herpes zoster involving the 1st division of the trigeminal nerve (V1 distribution – forehead, periocular area, & nose)
• Herpes zoster oticus (Ramsay Hunt syndrome): Herpes zoster involving the geniculate ganglion w/ rash including the ear, hard palate, or anterior two-thirds of the tongue in conjunction w/ involvement of CN VII (ipsilateral facial nerve palsy) & variable other CN findings (tinnitus, hearing loss, N/V, vertigo, nystagmus, etc.)
• Ramsay Hunt syndrome zoster sine herpete: Clinical features similar to RHS w/o rash.
History
• Previous varicella infection, localized abnl skin sensations (tingling, hot/cold sensation, pruritus, burning pain) prior to rash
• Pts may experience prodromal HA, photophobia, malaise
• RFs: Increasing age, immunosuppressive meds (ie, corticosteroids), neoplastic dz (esp lymphoproliferative cancers), & organ-transplant recipients, HIV
Physical Findings
• Grouped vesicles on erythematous base → crusted lesions, dermatomal distribution (pathognomonic), doesn’t cross midline. Note, lesions overlap adjacent dermatomes in up to 20% of cases.
Treatment
• Therapy should be started w/i 72 h of onset of lesions, but should still be considered if new vesicles are still forming after this period
• Therapy should be initiated in ALL pts who have herpes zoster ophthalmicus, are immunocompromised, or older in age regardless of timing of presentation
• Antivirals (valacyclovir, acyclovir, famciclovir) decreased course & neuralgic pain
• Acyclovir 800 mg PO q4h 5 times daily × 7–10 d
• Valacyclovir 1000 mg PO q8h × 7 d
• Famciclovir 500 mg PO q8h × 7 d
• Corticosteroids may accelerate rate of cutaneous healing & alleviate pain, but have no effect on incidence of postherpetic neuralgia
• Symptomatic (pain control w/ NSAIDs or opiates)
Disposition
• Home
• Pts w/ herpes zoster ophthalmicus should have f/u w/ ophthalmology
Pearls
• Cx: Encephalitis, myelitis, cranial & peripheral nerve palsies, a syndrome of delayed contralateral hemiparesis, pneumonitis, hepatitis, & acute retinal necrosis. In herpes zoster ophthalmicus, up to 50% pts can have ocular cx (ie, iritis, episcleritis, or keratopathy) if untreated.
• Can be disseminated in severe cases/immunocompromised
• Postherpetic neuralgia occurs when pain persists >30 d after onset of rash, & prevalence increases w/ age
Pityriasis Rosea (associated HHV-6 and HHV-7)
Definition
• Acute, self-healing exanthema thought to be a/w HHV-6 & HHV-7
• Lasts about 45 d (range 2 wk–5 mo)
• A/w asthma, eczema, recent URIs
History
• May be more frequent in cold seasons & clustering of cases can also be seen
• May be a/w constitutional sxs: Malaise, nausea, HA, irritability, anorexia, joint pain, URI/GI sxs, sore throat, low-grade fever
• Mild pruritus
Physical Findings
• May present only w/ “Herald patch” which is oval, pink/salmon color & elevated patch w/ fine scaling borders & pale, depressed center. May remain isolated for 2 wk prior to eruption. May precede initial rash in 50% cases.
• Check axillae, groin & perineum as it may be hidden.
• Multiple small pink/salmon, oval-shaped, patches similar in appearance to herald patch on trunk & prox. extremities (“Christmas tree pattern”); spares face, scalp, palms, & soles typically, but can be present in 15–20%.
Treatment
• Symptomatic (oatmeal baths & emollients may help, but unlikely to benefit)
Disposition
• Home
Molluscum Contagiosum (associated Poxvirus)
Definition
• Benign, self-limiting epidermal eruption caused by poxvirus that may last months to years
• Can serve as marker or opportunistic infection in pts w/ HIV
• Transmitted through fomite, skin-to-skin contact, & sexual contact
• Autoinnoculation may occur
History
• Nonpainful, nonpruritic rash
Physical Findings
• Firm, smooth, dome-shaped papules (2–5 mm) w/ umbilicated center, most common on face, trunk, & extremities, but can be found in axilla, antecubital/popliteal fossa, genitals
Treatment
• Self-limited, no tx needed
• Lesion eradication can be performed to decrease risk of autoinoculation (cryotherapy, laser, curettage, imiquimod cream, trichloroacetic acid, or tretinoin)
Disposition
• Home
BACTERIAL EXANTHEMS
Scarlet Fever (Scarlatina, “Second Disease”)
Definition
• Rash in children (3–12 y/o) caused by gram+, erythrogenic, toxin-producing strains of group A β-hemolytic streptococci.
• Transmitted via airborne droplets from those w/ active dz or asymptomatic carriers as well as via fomites
History
• More prevalent in temperate climates & in early winter/spring
• Incubation period 1–4 d followed by acute onset sore throat, fever, HA, vomiting, then rash 1–2 d after sore throat. Abdominal pain may also be present & severe.
Physical Findings
• Red/scarlet colored macules on background of diffuse erythema w/ finely punctate lesions of “goose-bump” appearance, “sandpaper” texture, starts on neck/axilla/groin → trunk/extremities/face (spares palms/soles)
• Distinctive features include circumoral pallor & increased intensity at skin folds; there are often transverse red streaks in skin folds known as Pastia’s lines
• Rash resolves w/i 1 wk followed by brawny desquamation 7–10 d later
• “Strawberry” tongue, beefy red pharynx & tonsils w/ or w/o exudative effusion palatal petechiae
Evaluation
• Rapid strep test (sens 60–90%, spec 90%), throat cultures
• CBC rarely indicated but usually leukocytosis w/ PMN predominance present
Treatment
• Penicillin VK QID × 10 d, benzathine penicillin 1.2 million U IM × 1, or erythromycin in penicillin-allergic pts
Disposition
• Home
Impetigo
Definition
• Highly contagious superficial epidermal infection affecting mainly children (2–5 y/o), & is the most common bacterial skin infection in children
• Caused by S. aureus & group A β-hemolytic streptococci
• 2 types: Nonbullous & bullous impetigo
• Nonbullous impetigo accounts for majority if cases & represents a host response to infection
• Bullous impetigo is caused by bacterial toxins, particularly staphylococcal exfoliative toxins
• Transmitted via direct contact, autoinnoculation, & fomites
History
• More prevalent in early summer months
Physical Findings
• Nonbullous impetigo: Begins as red macule or papule that becomes a vesicle. Vesicle ruptures to form an erosion & its contents dry, forming honey-colored crusts; usually on face (cheeks or under lips) or extremities; self-limited over 2 wk.
• Bullous impetigo: Begins as rapidly enlarging vesicles that form sharply demarcated bullae w/ little to no surrounding erythema. These rupture, forming yellow oozing crusts; usually moist intertriginous areas involved (neck fold, axilla, groin, perineum); self-limited.
Evaluation
• Dx is clinical; gram stain & culture rarely indicated
Treatment
• Supportive care as most will resolve spontaneously
• Topical abx: Mupirocin 2% ointment to affected area TID for 3–5 d
• Oral abx may be indicated in those who cannot tolerate topical tx or w/ extensive dz: Amoxicillin/clavulanate, dicloxacillin, cephalexin, erythromycin for pen-allergic pts.
• Cx: Poststrep glomerulonephritis, cellulitis, lymphangitis, TSS, SSSS, osteomyelitis, arthritis, sepsis, endocarditis
Disposition
• Home
• Instruction to prevent spreading
(Refer to Chapter 4, “Soft Tissue Infections” for other bacterial exanthems: Erysipelas, Cellulitis, Staphylococcal Scalded Skin Syndrome, Toxic Shock Syndrome, and Necrotizing Fascitis)
FUNGAL EXATHEMS
Dermatophytoses
Definitions
• All denote superficial fungal infections (mycoses) involving the stratum corneum, hair, or nails; more specifically termed dermatophytoses
• Tinea capitis describes dermatophyte infection of hair & scalp caused by Trichopyton & Microsporum species
• Tinea corporis refers to any dermatophytosis of glabrous (smooth, hairless) skin except palms, soles, & the groin region. Most commonly caused by T. rubrum.
• Tinea cruris is a dermatophytosis of the groin, genitals, pubic area, or perineum. Most commonly caused by T. rubrum or E. floccosum.
• Tinea pedis describes dermatophytosis of the feet, while tinea manuum involves the hand (commonly the palms or interdigital regions). Most commonly caused by T. rubrum, T. interdigitale, or E. floccosum.
• Tinea unguium/Onychomycosis describe fungal infections of the nail. Most commonly caused by T. rubrum, T. interdigitale, or E. floccosum.
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