76 The Canadian Journal of Diagnosis / August 2001

IdentifyingInfectiousRashes inChildren

IdentifyingInfectiousRashes inChildren

By Rupesh Chawla, MD, FRCPC; Herbert Dele Davies, MD,FRCPC; and Taj Jadavji, MD, FRCPC

Rash is the most common condition withwhich children present, alongside aparent, to their physicians office. There aremultiple types of rash in childhood includinginfectious, allergic, contact-reactions,autoimmune and neoplasmic. This articlewill focus on those rashes that occur in chil-dren outside the neonatal period, secondaryto an infectious etiology.

Infectious rashes can be subdivided intothose caused by viruses, bacteria and othermiscellaneous infectious agents. As is true ofmost infectious conditions in children, themost common etiology for infectious rash isa viral infection.

To diagnose the etiology of a rash, a com-plete history and physical examination isrequired. There is a story to every rash. Thehistory of the rash should focus on rash pro-gression (Table 1), associated symptoms(Table 2) and exposures (Table 3).

Viral Exanthems

Maculopapular RashesRubeola/measles.Measles used to be an epi-demic disease. Fortunately, with immuniza-tion, it is now seen infrequently. The incuba-tion period for rubeola after contact is eight to12 days to the onset of prodromal symptoms

With the typical child contracting many rashes, it isimportant for the family physician to know which rashesare infectious and which are not.

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and 14 days to onset of rash. The prodrome isthree to five days in duration, and includesenanthem (Koplik spots), fever, cough,coryza and conjunctivitis.

The rash of measles begins as macular andprogresses to maculopapular (with or withoutpetechiae). In severe cases, a confluent rashcan occur, which includes the palms andsoles. There is slight pruritis associated withthe rash. The rash begins at neck, hairline,behind ears and the posterior cheek. Thecharacteristic spread is: Day 1: Face, neck, upper arms, upper

chest; Day 2: Back, abdomen, entire arms, and

thighs; Day 3: Feet and begins to fade on face; Days 4 and 5: Symptoms subside;

desquamation and discoloration occurafter the rash fades.

Rubella. This has an incubation period of 14to 23 days after contact. The prodrome is ofmild catarrhal symptoms for a few days andlymphadenopathy at least 24 hours prior torash. The rash is maculopapular, with areas offlushing. The rash has rapid evolution andrapid fading (it classically clears by the thirdday). Spread of the rash is from the face to thetrunk. There may or may not be associatedmild pruritis.

Parvovirus B19.The incubation period forparvovirus is four to 14 days (and could be aslong as 21 days). There is a brief non-specif-ic illness with fever, malaise, myalgias andheadache as a prodrome. The facial rash isintensely red with a slapped cheek appear-ance, with or without circumoral pallor.There also is a symmetric maculopapularlacy rash on the trunk. The rash then movesperipherally to the arms, thighs and buttocks.The rash often is pruritic.Roseola/HHV-6.The incubation period forHHV-6 is nine to 10 days. The prodrome is ahigh-grade fever for three to seven days. Therash is erythematous and maculopapular, last-ing hours to days.

Dr. Dele Davies is associate professor, departmentsof pediatrics, microbiology and infectious diseases,Alberta Childrens Hospital, University of Calgary, anddirector, child health research unit, AlbertaChildrens Hospital, Calgary, Alberta.

Dr. Jadavji is professor, departments of pediatrics,microbiology and infectious diseases, University ofCalgary, and associate dean, international healthprogram, University of Calgary. He also is head,division of infectious diseases, Alberta ChildrensHospital, Calgary, Alberta.

Dr. Chawla is pediatric infectious disease fellow,Alberta Childrens Hospital, University of Calgary,Calgary, Alberta.

Adenoviruses.These cause a variety of dif-ferent manifestations including: respiratorytract infections, gastroenteritis, conjunctivitisand cystitis. These viruses also can cause amaculopapular rash in patients.

Epstein-Barr Virus and Cytomegalovirus.These can cause mononucleosis-like syn-dromes and lead to a maculopapular rashafter treatment with antibiotics (especiallywith amoxicillin.

Vesicular RashesHerpes Simplex Virus (I and II).These virus-es lead to a characteristically painful vesicu-lar lesion that can be oral-labial (herpes sim-plex virus type I [HSV-I] majority) or genital(HSV-II). The lesions can be predicted by the

sensation of tingling priorto a breakout. HSV alsocan cause gingivostomati-tis, eczema herpeticum,herpetic whitlow, conjunc-tivitis and keratitis. Thereare primary infections withsubsequent secondaryreactivations from thenerve root, which tend tobe less severe than the pri-mary outbreak).

Varicella zoster (chicken pox and shingles).Primary infection caused by the varicellazoster virus causes chicken pox. The incuba-tion period is 14 to 16 days (from 10 to 21days after contact). The rash of chicken poxis generalized, pruritic and goes through dif-ferent stages. The rash is initially macu-

lopapular, then goes to a vesicular stage andthen crusts over. The patient with chickenpox often will have different stages of therash presenting at once. Hemorrhagic chick-en pox occurs more commonly in theimmunocompromised host. Secondary bacte-rial infections of the chicken pox lesions(e.g.,cellulitis) are the most common com-plication. Necrotizing fasciitis, an infectionsecondary to Group AStreptococcus,although rare, is highly associated withchicken pox. The varicella zoster virusbecomes latent in the dorsal root ganglion.Reactivation of the virus leads to herpeszoster or shingles. The rash appears along thedermatome supplied by the dorsal root thatwas reactivated. The rash is vesicular and ispainful. The pain can persist beyond onemonth (post-herpetic neuralgia).

Enteroviruses (Coxsackie A16 andenterovirus 71 [hand, foot and mouth dis-ease]). These summer viruses present asvesicular lesions with a predilection for the

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The Canadian Journal of Diagnosis / August 2001

Table 1

RASH PROGRESSION

Where did the rash start?

Sequence of the rash?

Type of rash?

Duration of onset?

Involvement of palms and soles?

Involvement of mucous membranes?

Involvement of conjunctiva?

+/- Strawberry tongue?

+/- Desquamating?

Adenoviruses areknown to causemaculopapularrashes inpatients.

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Infectious Rashes

hand, feet and mouths of affected patients.The illness is self-limited, with total recovery.Lesions can be painful enough to preventnormal eating and drinking in the affectedpatient.

Other Rashes Molluscum contagiosum.The poxvirus caus-es molluscum contagiosum. The lesions aresmall, discrete and flesh-colored to translu-cent dome-shaped papules, which often havecentral umbilication. The lesions occur mostcommonly on the trunk, face and extremities,but can be generalized.

Warts (human papilloma virus).The humanpapilloma viruses lead to epithelial tumors(warts) of skin and mucous membranes. Thelesions appear as dome-shaped, with conicalprojections that give a rough appearance. Thelesions tend to be asymptomatic and self-lim-ited.

Bacterial Infections

Staphylococcal InfectionsStaphylococcus aureusis responsible forcausing rashes in children. The conditionsthat staphylococcus can cause include:

Impetigo.This lesion begins as apapule, which rapidly evolves into avesicle surrounded by an area of erythe-ma. Vesicular lesions give rise to pus-tules that gradually enlarge and thenbreak down over four to six days toform characteristically thick crusts(golden). They occur at sites of non-

intact skin. Staphylococcuscan causebullous and non-bullous forms ofimpetigo.

Cellulitis. This is a painful, erythematousand indurated infection of the skin andsoft tissues. It often presents after an ini-tial injury to the patients skin, and isassociated with lymphangitis and lym-phadenopathy.

Staphylococcal scalded skin syndrome.This syndrome is caused by toxins (exfo-

The Canadian Journal of Diagnosis / August 2001

Table 2

ASSOCIATED SIGNS AND SYMPTOMS

Fever

Cough

Coryza

Conjunctivitis

Rhinorrhea

Sore throat

Mucositis

Tongue changes (e.g., strawberry)

Lymphadenopathy

Nausea/vomiting

Abdominal pain

Diarrhea

Pruritis

Pain (quality and severity)

Weakness

Dizziness

Headache

Swollen extremities

liative toxin A and B) released by certainS. aureusstrains. Its initial presentation isof fever, generalized erythema and skintenderness. Within 24 hours, affectedskin gathers into folds, forming superfi-cial blisters, and when the blisters rup-ture, the skin peels off in sheets, leavinga moist, painful, red base.

Staphylococcal toxic shock syndrome.This is an acute, multisystem diseasewith high fever, hypotension, vomiting,abdominal pain, diarrhea, myalgias, non-focal neurologic abnormalities and anerythematous rash. The rash is diffuse,red and macular (sunburn-like) andappears within 24 hours. There may beassociated hyperemia of the mucous

membranes. There maybe petechiae on daysthree and four of theillness. After resolu-tion, there is associateddesquamation, espe-cially of the palms andsoles.

Group A Streptococcal(GAS) InfectionsGAS is responsible forthe following condi-

tions in children:

Impetigo.GAS causes non-bullousimpetigo associated with honey-crustedlesions on skin, particularly around thenares.

Scarlet fever. This is caused by a strain ofGAS that produces an erythrogenic toxin.The clinical manifestation includes fever,headache with or without vomiting, andfacial flushing with marked circumoralpallor. The rash lasts four to 10 days,starts on the second clinical day of illnesson the trunk and spreads to the extremi-ties. The palms, soles and face are spared,and the rash has a sandpaper-like texture.

The skin in the cutaneous folds of theneck and anterior groin may developincreased prominence and show as darkred lines (Pastias lines).

Strawberry tongue may be present. Oneto two weeks after the onset of illness,the skin will begin to peel. This may lastseveral weeks.

Cellulitis. The description is similar tothe description for S. aureus.

Erysipelas.This is a deep infection of theskin, usually on the face, with markedlymphoid involvement. The patient is

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Table 3

ASSOCIATED EXPOSURES

Immunizations

Pets

Foreign travel

Bites (insects/ticks)

Carpet cleaning (Kawasaki disease)

Recent injuries with cuts or scrapes

Sexual history

Sick contacts

The conditions thatstaphylococcus cancause includeimpetigo, cellulitis,and staphylococcalscalded skinsyndrome.

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usually febrile and the skin is doughy tothe touch.

Rheumatic fever.Erythema marginatumoccurs very infrequently. Early in the dis-ease it presents as pink macules over thetrunk. Later, there is blanching in themiddle of the lesions, with fusing of theborders and leads to a serpiginous-look-ing lesion.

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

Necrotizing fasciitis. This is a deep-seat-ed infection of the subcutaneous tissuesresulting in progressive destruction offascia and fat. It may occur as a compo-nent of STSS or among patients with nosigns of shock/organ failure. It may ormay not have muscle involvement(myositis).

Meningococcal infectionsmeningococcemia/purpura fulminansNeisseria meningitidis causes a life-threatening condition known as meningococ-cemia, which is a blood-stream infection withthe pathogen. The rash of meningococcemiais one that no one should ignore. The rash,however, can initially begin non-specificallyas maculopapular or urticarial in nature. Theclassic non-blanching petechiae also can bethe presenting rash. These can coalesce todevelop into purpura (Figure 1.) The onset ofthis infection is abrupt, with fever, chills,

malaise and rash. The misdiagnosis of thisrash will lead to patient mortality and mor-bidity.

Other Infections

Lyme disease (erythema chronicummigrans)Lyme disease is secondary to infection by thespirocheteBorrelia burgoderferi.The spiro-chetre is transmitted to humans by a tick bite.The skin is the initial target of infection andinflammation, which leads to the characteris-tic rash: annular rash occurs seven to 14 daysafter bite (from three to 32 days). The initiallesion is usually at the site of the bite, andmay be uniformly erythematous or a targetlesion with central clearing or central vesicu-lar/necrotic areas (average diameter 15 cm).

Infectious Rashes

The Canadian Journal of Diagnosis / August 2001

Figure 1. An example of purpura.

In the secondary stage, skin lesions canappear, which are smaller and secondary tothe migration of the spirochete.

SyphilisThis infection is sexually transmitted, sec-ondary to the spirochete Treponema pal-lidum. In primary syphilis, a painlesschanchre occurs on the genitals with regionallymphadenopathy. In secondary syphilis, ageneralized skin eruption that is maculopapu-lar (scaling) occurs on the head, neck, palmsand soles.

Rocky Mountain Spotted FeverThe spirochete Rickettsia rickettsiicausesRocky Mountain Spotted Fever. A tick, thenatural host and reservoir, introduces thespirochete to humans by a bite. Initially,patients complain of headache, fever, anorex-ia and restlessness. The third day after a bite,a skin rash appears which, initially, is macu-lopapular on the extremities and then spreadsover the entire body. The rash subsequentlybecomes more petechial or hemorrhagic innature.

Scabies This is a skin infestation by a mite. The rashis an erythematous papular eruption and canbe vesicular in children under two years ofage. The rash is intensely pruritic, especiallyat night. The skin manifestation is secondaryto a hypersensitivity reaction to the proteinsof the mite. Transmission of the mite is skinto skin. If scabies is suspected, one must lookfor the mite burrows. Bacteria may secondar-ily infect the bites.

Kawasaki Disease (Atypical mucocutaneouslymph node syndrome)Kawasaki disease is of unknown etiology butinfectious and post-infectious etiologies arepostulated. Typical Kawasaki diseaserequires a five-day history of fever with fourof the following five criteria presenting: Rash of any type (non-vesicular); Cervical lymphadenopathy more than 1.5

cm; Mucositis: dry, red cracked lips and

strawberry tongue; Swollen hands and feet (especially tips),

which progresses to peeling; and Bilateral non-purulent conjunctivitis.

Atypical disease may have fewer criteriapresent. Treatment for Kawasaki disease is toprevent or reverse coronary aneurysm forma-tion.

Suggested Readings1. Pickering LK: 2000 Red Book: Report of the Committee on

Infectious Diseases. 25th Edition. American Academy ofPediatrics, Illinois, 2000.

2. Ladhani S, Joannou CL, Lochrie DP, et al: Clinical, microbial,and biochemical aspects of the exfoliative toxins causingstaphylococcal scalded-skin syndrome. Clin Microbiol Rev1999; 12:224-42.

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