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Infectious Rashesrashes Inin Childrenchildren IdentifyingIdentifying InfectiousInfectious RashesRashes inin ChildrenChildren With the typical child contracting many rashes, 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 rash, a com- R which children present, alongside a plete history and physical examination 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. 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 76 The Canadian Journal of Diagnosis / August 2001 Infectious Rashes and 14 days to onset of rash. The prodrome is Rubella. 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 flushing. 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 face 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: Parvovirus B19. 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; headache 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. desquamation 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. The Canadian Journal of Diagnosis / August 2001 77 Infectious Rashes 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 tongue? •+/- 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 [hand, 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 78 The Canadian Journal of Diagnosis / August 2001 Infectious Rashes hand, feet and mouths of affected patients. Table 2 The illness is self-limited, with total recovery. ASSOCIATED SIGNS AND SYMPTOMS 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 • Diarrhea papilloma viruses lead to epithelial tumors •Pruritis (warts) of skin 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- The Canadian Journal of Diagnosis / August 2001 79 Infectious Rashes 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 shock 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 • Scarlet fever. 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
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