IdentifyingIdentifying InfectiousInfectious RashesRashes inin ChildrenChildren

With the typical child contracting many , it is important for the family physician to know which rashes are infectious and which are not. By Rupesh Chawla, MD, FRCPC; Herbert Dele Davies, MD, FRCPC; and Taj Jadavji, MD, FRCPC

ash is the most common condition with To diagnose the etiology of a , a com- R which children present, alongside a plete history and is parent, to their physician’s office. There are required. There is a “story” to every rash. The multiple types of rash in childhood including history of the rash should focus on rash pro- infectious, allergic, contact-reactions, gression (Table 1), associated symptoms autoimmune and neoplasmic. This article (Table 2) and exposures (Table 3). will focus on those rashes that occur in chil- dren outside the neonatal period, secondary Viral Exanthems to an infectious etiology. Infectious rashes can be subdivided into Maculopapular Rashes those caused by viruses, bacteria and other Rubeola/. Measles used to be an epi- miscellaneous infectious agents. As is true of demic disease. Fortunately, with immuniza- most infectious conditions in children, the tion, it is now seen infrequently. The incuba- most common etiology for infectious rash is tion period for rubeola after contact is eight to a viral infection. 12 days to the onset of prodromal symptoms

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and 14 days to onset of rash. The prodrome is . This has an incubation period of 14 three to five days in duration, and includes to 23 days after contact. The prodrome is of enanthem (Koplik spots), fever, cough, mild catarrhal symptoms for a few days and coryza and conjunctivitis. lymphadenopathy at least 24 hours prior to The rash of measles begins as macular and rash. The rash is maculopapular, with areas of progresses to maculopapular (with or without . The rash has rapid evolution and petechiae). In severe cases, a confluent rash rapid fading (it classically clears by the third can occur, which includes the palms and day). Spread of the rash is from the to the soles. There is slight pruritis associated with trunk. There may or may not be associated the rash. The rash begins at neck, hairline, mild pruritis. behind ears and the posterior cheek. The characteristic spread is: . The incubation period for •Day 1: Face, neck, upper arms, upper parvovirus is four to 14 days (and could be as chest; long as 21 days). There is a brief non-specif- •Day 2: Back, abdomen, entire arms, and ic illness with fever, malaise, myalgias and thighs; as a prodrome. The facial rash is •Day 3: Feet and begins to fade on face; intensely red with a “slapped cheek” appear- •Days 4 and 5: Symptoms subside; ance, with or without circumoral pallor. and discoloration occur There also is a symmetric maculopapular after the rash fades. lacy rash on the trunk. The rash then moves peripherally to the arms, thighs and buttocks. The rash often is pruritic. Roseola/HHV-6. The incubation period for Dr. Chawla is pediatric infectious disease fellow, HHV-6 is nine to 10 days. The prodrome is a Alberta Children’s Hospital, University of Calgary, Calgary, Alberta. high-grade fever for three to seven days. The rash is erythematous and maculopapular, last- ing hours to days.

Dr. Jadavji is professor, departments of pediatrics, Dr. Dele Davies is associate professor, departments microbiology and infectious diseases, University of of pediatrics, microbiology and infectious diseases, Calgary, and associate dean, international health Alberta Children’s Hospital, University of Calgary, and program, University of Calgary. He also is head, director, child health research unit, Alberta division of infectious diseases, Alberta Children’s Children’s Hospital, Calgary, Alberta. Hospital, Calgary, Alberta.

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Adenoviruses. These cause a variety of dif- Table 1 ferent manifestations including: respiratory RASH PROGRESSION tract infections, gastroenteritis, conjunctivitis • Where did the rash start? and cystitis. These viruses also can cause a maculopapular rash in patients. •Sequence of the rash? •Type of rash? Epstein-Barr Virus and Cytomegalovirus. • Duration of onset? These can cause mononucleosis-like syn- • Involvement of palms and soles? dromes and lead to a maculopapular rash • Involvement of mucous membranes? after treatment with antibiotics (especially • Involvement of conjunctiva? with amoxicillin. •+/- Strawberry ? •+/- Desquamating? Vesicular Rashes Herpes Simplex Virus (I and II). These virus- es lead to a characteristically painful vesicu- lopapular, then goes to a vesicular stage and lar lesion that can be oral-labial (herpes sim- then crusts over. The patient with chicken plex virus type I [HSV-I] majority) or genital pox often will have different stages of the (HSV-II). The lesions can be predicted by the rash presenting at once. Hemorrhagic chick- sensation of tingling prior en pox occurs more commonly in the to a breakout. HSV also immunocompromised host. Secondary bacte- can cause gingivostomati- rial infections of the chicken pox lesions Adenoviruses are tis, eczema herpeticum, (e.g., cellulitis) are the most common com- herpetic whitlow, conjunc- plication. Necrotizing fasciitis, an infection known to cause tivitis and keratitis. There secondary to Group A Streptococcus, maculopapular are primary infections with although rare, is highly associated with subsequent secondary chicken pox. The varicella zoster virus rashes in reactivations from the becomes latent in the dorsal root ganglion. patients. nerve root, which tend to Reactivation of the virus leads to herpes be less severe than the pri- zoster or shingles. The rash appears along the mary outbreak). dermatome supplied by the dorsal root that was reactivated. The rash is vesicular and is Varicella zoster (chicken pox and shingles). painful. The pain can persist beyond one Primary infection caused by the varicella month (post-herpetic neuralgia). zoster virus causes chicken pox. The incuba- tion period is 14 to 16 days (from 10 to 21 Enteroviruses (Coxsackie A16 and days after contact). The rash of chicken pox enterovirus 71 [, foot and mouth dis- is generalized, pruritic and goes through dif- ease]). These summer viruses present as ferent stages. The rash is initially macu- vesicular lesions with a predilection for the

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hand, feet and mouths of affected patients. Table 2 The illness is self-limited, with total recovery. ASSOCIATED Lesions can be painful enough to prevent • Fever normal eating and drinking in the affected patient. • Cough •Coryza Other Rashes •Conjunctivitis Molluscum contagiosum. The poxvirus caus- • Rhinorrhea es molluscum contagiosum. The lesions are • Sore throat small, discrete and flesh-colored to translu- • Mucositis cent dome-shaped papules, which often have •Tongue changes (e.g., strawberry) central umbilication. The lesions occur most •Lymphadenopathy commonly on the trunk, face and extremities, •Nausea/vomiting but can be generalized. • Abdominal pain

Warts (human papilloma virus). The human • papilloma viruses lead to epithelial tumors •Pruritis (warts) of and mucous membranes. The •Pain (quality and severity) lesions appear as dome-shaped, with conical •Weakness projections that give a rough appearance. The • Dizziness lesions tend to be asymptomatic and self-lim- •Headache ited. • Swollen extremities

Bacterial Infections Staphylococcal Infections intact skin. Staphylococcus can cause Staphylococcus aureus is responsible for bullous and non-bullous forms of causing rashes in children. The conditions impetigo. that staphylococcus can cause include: •Cellulitis. This is a painful, erythematous •Impetigo. This lesion begins as a and indurated infection of the skin and papule, which rapidly evolves into a soft tissues. It often presents after an ini- vesicle surrounded by an area of erythe- tial injury to the patient’s skin, and is ma. Vesicular lesions give rise to pus- associated with lymphangitis and lym- tules that gradually enlarge and then phadenopathy. break down over four to six days to form characteristically thick crusts • Staphylococcal scalded skin syndrome. (golden). They occur at sites of non- This syndrome is caused by toxins (exfo-

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liative toxin A and B) released by certain Table 3 S. aureus strains. Its initial presentation is ASSOCIATED EXPOSURES of fever, generalized erythema and skin tenderness. Within 24 hours, affected •Immunizations skin gathers into folds, forming superfi- •Pets cial blisters, and when the blisters rup- • Foreign travel ture, the skin peels off in sheets, leaving • Bites (insects/ticks) a moist, painful, red base. • Carpet cleaning (Kawasaki disease) • Recent injuries with cuts or scrapes • Staphylococcal toxic syndrome. • Sexual history This is an acute, multisystem disease •Sick contacts with high fever, hypotension, vomiting, abdominal pain, diarrhea, myalgias, non- focal neurologic abnormalities and an • . This is caused by a strain of erythematous rash. The rash is diffuse, GAS that produces an erythrogenic toxin. red and macular (sunburn-like) and The clinical manifestation includes fever, appears within 24 hours. There may be headache with or without vomiting, and associated hyperemia of the mucous facial flushing with marked circumoral membranes. There may pallor. The rash lasts four to 10 days, be petechiae on days starts on the second clinical day of illness The conditions that three and four of the on the trunk and spreads to the extremi- staphylococcus can illness. After resolu- ties. The palms, soles and face are spared, tion, there is associated and the rash has a sandpaper-like texture. cause include desquamation, espe- The skin in the cutaneous folds of the impetigo, cellulitis, cially of the palms and neck and anterior groin may develop soles. increased prominence and show as dark and staphylococcal red lines (Pastia’s lines). scalded skin Group A Streptococcal Strawberry tongue may be present. One (GAS) Infections to two weeks after the onset of illness, syndrome. GAS is responsible for the skin will begin to peel. This may last the following condi- several weeks. tions in children: • Cellulitis. The description is similar to • Impetigo. GAS causes non-bullous the description for S. aureus. impetigo associated with honey-crusted lesions on skin, particularly around the • Erysipelas. This is a deep infection of the nares. skin, usually on the face, with marked lymphoid involvement. The patient is

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usually febrile and the skin is doughy to the touch.

• Rheumatic fever. Erythema marginatum occurs very infrequently. Early in the dis- ease it presents as pink macules over the trunk. Later, there is blanching in the middle of the lesions, with fusing of the borders and leads to a serpiginous-look- ing lesion.

• Streptococcal toxic shock syndrome (STSS). Patients develop rapidly progres- sive hypotension and multisystem organ failure.

• Necrotizing fasciitis. This is a deep-seat- Figure 1. An example of purpura. ed infection of the subcutaneous tissues resulting in progressive destruction of fascia and fat. It may occur as a compo- malaise and rash. The misdiagnosis of this nent of STSS or among patients with no rash will lead to patient mortality and mor- signs of shock/organ failure. It may or bidity. may not have muscle involvement (myositis). Other Infections Meningococcal infections— Lyme disease (erythema chronicum meningococcemia/purpura fulminans migrans) Neisseria meningitidis causes a life- Lyme disease is secondary to infection by the threatening condition known as meningococ- spirochete Borrelia burgoderferi. The spiro- cemia, which is a blood-stream infection with chetre is transmitted to humans by a tick bite. the pathogen. The rash of meningococcemia The skin is the initial target of infection and is one that no one should ignore. The rash, inflammation, which leads to the characteris- however, can initially begin non-specifically tic rash: annular rash occurs seven to 14 days as maculopapular or urticarial in nature. The after bite (from three to 32 days). The initial classic non-blanching petechiae also can be lesion is usually at the site of the bite, and the presenting rash. These can coalesce to may be uniformly erythematous or a target develop into purpura (Figure 1.) The onset of lesion with central clearing or central vesicu- this infection is abrupt, with fever, chills, lar/necrotic areas (average diameter 15 cm).

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In the secondary stage, skin lesions can Kawasaki Disease (Atypical mucocutaneous appear, which are smaller and secondary to lymph node syndrome) the migration of the spirochete. Kawasaki disease is of unknown etiology but infectious and post-infectious etiologies are postulated. Typical Kawasaki disease This infection is sexually transmitted, sec- requires a five-day history of fever with four ondary to the spirochete Treponema pal- of the following five criteria presenting: lidum. In primary syphilis, a painless • Rash of any type (non-vesicular); chanchre occurs on the genitals with regional • Cervical lymphadenopathy more than 1.5 lymphadenopathy. In secondary syphilis, a cm; generalized skin eruption that is maculopapu- • Mucositis: dry, red cracked and lar (scaling) occurs on the head, neck, palms strawberry tongue; and soles. • Swollen and feet (especially tips), which progresses to peeling; and Rocky Mountain Spotted Fever •Bilateral non-purulent conjunctivitis. The spirochete Rickettsia rickettsii causes Atypical disease may have fewer criteria Rocky Mountain Spotted Fever. A tick, the present. Treatment for Kawasaki disease is to natural host and reservoir, introduces the prevent or reverse coronary aneurysm forma-

spirochete to humans by a bite. Initially, tion. Dx patients complain of headache, fever, anorex- Suggested Readings ia and restlessness. The third day after a bite, 1. Pickering LK: 2000 Red Book: Report of the Committee on a skin rash appears which, initially, is macu- Infectious Diseases. 25th Edition. American Academy of Pediatrics, Illinois, 2000. lopapular on the extremities and then spreads 2. Ladhani S, Joannou CL, Lochrie DP,et al: Clinical, microbial, and biochemical aspects of the exfoliative toxins causing over the entire body. The rash subsequently staphylococcal scalded-skin syndrome. Clin Microbiol Rev becomes more petechial or hemorrhagic in 1999; 12:224-42. nature.

Scabies This is a skin infestation by a mite. The rash is an erythematous papular eruption and can be vesicular in children under two years of age. The rash is intensely pruritic, especially at night. The skin manifestation is secondary to a hypersensitivity reaction to the proteins of the mite. Transmission of the mite is skin to skin. If scabies is suspected, one must look for the mite burrows. Bacteria may secondar- ily infect the bites.

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