Strange and Schafermeyer's Pediatric Emergency Medicine, Fourth Edition (Strange, Pediatric Emergency Medicine), 4th Ed.

CHAPTER 91. Viral Exanthems

Arianna Shirk

Annalise Sorrentino


• Most childhood exanthems are benign, self-limited, and require no treatment; but hidden in this presentation is an occasional myocarditis, encephalitis, or pneumonia.

• Worldwide, rubeola is still a major cause of morbidity and mortality. Early recognition can control spread.

• Roseola infantum is a common cause of febrile seizures in infants. A full fontanelle may be present in up to 25%.

• Children with varicella that may benefit from antiviral agents include patients on corticosteroids or chronic salicylates, immunocompromised patients, and those older than 12 years.

• Neonatal herpes has three presentations in the first 6 weeks of life: Encephalitis with seizures, disseminated with a “neonatal sepsis” appearance, and those localized to the skin, eye(s), and mouth. Early treatment with acyclovir will prevent progression.


The vast majority of childhood exanthems are a result of nonspecific, self-limited viral illnesses. However, recognizing their patterns being familiar with the history and physical findings associated with these specific exanthems can be crucial to reassuring families, educating, and directing care.

The clinician should always be vigilant to recognize associated symptoms that may suggest life-threatening complications when examining children with exanthems. This chapter will describe recognizable childhood exanthems, discuss risks of exposure, and provide an understanding of complications to expect and serious sequelae to consider.



Rubeola, more commonly known as measles, is one of the most contagious diseases known to man with a 90% transmission rate to an unimmunized household contact. Although, widespread use of live virus vaccine during the past 40 years has dramatically reduced the incidence of the disease in developed countries, measles still remains a leading cause of preventable childhood morbidity and mortality worldwide. In 2010, measles resulted in 139,300 deaths worldwide, with more than 95% of these deaths occurred in developing countries. Maternally acquired antibodies usually are sufficient to protect against clinical exposure in infants younger than 1 year of age. In the United States, the AAP recommends vaccination with MMR (Measles, Mumps, Rubella) between 12 to 15 months of age and a second dose at 5 years. In 2010, 85% of the world’s children received at least one dose of the measles vaccines before their first birthday. Because of a successful vaccination campaign, most cases today are limited to immunocompromised patients and patients in developing countries where poverty and malnutrition is a factor.1

Transmission of the virus is by aerosol exposure or contact with respiratory fluids. The virus enters the body through the respiratory tract, and the incubation period ranges from 7 to 18 days after exposure. Patients are contagious for approximately 5 days after onset of symptoms, which usually begin with fever.


The characteristic measles rash is usually preceded by 3 days of fever to 40°C and the characteristic “three Cs“—cough, coryza, and conjunctivitis. Intense mucoid nasal drainage, hacking cough, and marked nonpurulent scleral and palpebral conjunctivitis are always present prior to the onset of rash. Koplik spots (Fig. 91-1A) are a characteristic enanthem that consists of blue–white discreet papules on the lateral buccal mucosa that are typically present during the early febrile period about 24 hours before onset of the generalized rash. By the time rash appears, Koplik spots may have coalesced into a white granular appearance or may be completely absent.


FIGURE 91-1. A. Koplik spots present 24 hours before and remain 24 hours after onset of rash. B. Rubeola exanthem at 3 days with coalescence.

The rash is a maculopapular erythematous rash that first appears on the face and spreads cephalocaudal to involve the trunk and extremities. At onset, it is discreet and maculopapular. By the third day, it begins to coalesce and becomes confluent as it turns from red to a yellow–brown color (Fig. 91-1B). The fever will resolve within 3 days of onset of rash, and, in uncomplicated cases, all symptoms should resolve within 7 to 8 days.


When rubeola is suspected, confirmatory diagnostic testing is necessary and can be done through contact with state public health laboratories or the Centers for Disease Control and Prevention (CDC). Measles IgM is usually present within 72 hours of the onset of rash and persists for at least 1 month. Examination of the saliva for measles-specific IgA and serum testing for a rise in IgG antibodies can also be used for diagnosis. Measles virus can also be isolated from respiratory secretions during the febrile period and identified by reverse transcription polymerase chain reaction (RT-PCR) or viral culture.2


The most common complication of rubeola is otitis media, occurring in up to 25% of children. Encephalitis will occur in approximately 1:1000 cases with outbreaks in developed countries. Serious complications such as pneumonia, diarrhea with dehydration, and blindness can be as high as 10% in poorly nourished children and 30% in the immunocompromised. Subacute sclerosing panencephalitis (SSPE) is a rare central nervous system degenerative disease that has virtually disappeared from the United States since widespread vaccination programs have been introduced.


Management is nonspecific supportive care for the uncomplicated patient. No antiviral agents proven to modify the course of measles. Administration of live virus vaccine may be beneficial in modifying the disease course when given within 72 hours of exposure. For children with history of immunodeficiency syndromes and HIV, pregnant women, and infant household contacts 6 to 12 months of age, 0.5 mL/kg of intravenous immunoglobulin (IVIG) is recommended within 6 days of exposure.3 Vitamin A supplementation may be helpful in preventing corneal ulcerations and blindness in malnourished children.4



In 2004, rubella was declared no longer endemic in the United States by the CDC. However, because outbreaks still occur in developing countries and with international travel, the clinician should be aware of the presentation and potential complications.

Humans are the only known host for transmission of rubella. Postnatal rubella is transmitted by airborne droplets from the upper respiratory tract. The virus has been shown to replicate in the nasopharynx and lymph nodes, and can be isolated from respiratory secretions, urine, feces, and skin. Transmission of disease can occur for approximately 1 week before the onset of rash until up to 14 days after symptoms appear. For exposed individuals, a single infection will induce lifetime immunity.

Because contagion is present before the appearance of the rash, widespread use of live attenuated virus vaccine has proven to be highly successful in reducing the morbidity associated with congenitally acquired rubella syndrome (CRS). Postnatally acquired rubella is generally mild and self-limited, but the effects of virus exposure on the fetus in the first 20 weeks of gestation (congenital rubella syndrome) have made it an important cause of congenitally acquired fetal morbidity and mortality. Congenital rubella syndrome is acquired by transplacental transfer of virus to the developing fetus during the first 20 weeks of gestation, and pregnant women should be screened to assess immunity to rubella.


The symptoms associated with postnatal rubella are usually mild, and it may be asymptomatic. Older children and adults usually present with 1- to 5-day prodrome of cough, coryza, and conjunctivitis. In young children, rash is usually the first symptom and prodrome is rare.

The characteristic maculopapular erythematous rash starts on the face and progresses cephalocaudally. The rash is usually pruritic and lasts up to 3 days. Pea-sized postauricular lymphadenopathy is usually seen by the time the rash appears. Symptoms usually resolve in 3 to 4 days.

The symptom complex can be differentiated from rubeola (measles) by the presence of a rash appearing at or near the onset of fever and the mild nature of symptoms. The rubella rash is also less prominent than the measles rash and usually does not coalesce.


Assays for detecting rubella immunity include enzyme immunoassay tests, immunofluorescent assay, and latex agglutination tests. Enzyme immunoassays for rubella-specific IgM antibodies are most commonly used tests to detect recent infection. Congenital rubella can be confirmed by persistent rubella-specific IgG antibody. IgG antibody titers can also be used to screen females of childbearing age.5


Complications from postnatal acquired rubella are rare and occur more commonly in adults. Transient polyarthralgias and polyarthritis occur in up to 70% of adult women. Thrombocytopenia is a more common lab abnormality and occurs in approximately 1:3000 cases. Encephalitis occurs in 1:6000 cases with headache, vomiting, stiff neck, and lethargy. These symptoms are usually self-limited without lasting sequelae. Orchitis and neuritis are rare, late-presenting symptoms.

Prevention of CRS is the main goal of rubella vaccination. Transplacentally acquired infections can result in birth defects, premature delivery, or fetal death caused by destruction of fetal cells and mitotic arrest. The extent of the effect is more significant when the mother is exposed during first 20 weeks of gestation. Patients with CRS can be recognized by the presence of hepatosplenomegaly, a “blueberry muffin rash,” microcephaly, and low birth weight. Cardiac anomalies, especially patent ductus arteriosus, are common. Cataracts, glaucoma, and retinopathy may be seen on eye examination. Hearing loss, mental retardation, growth delays, and learning disabilities may present later.6


Symptomatic treatment is all that is necessary for postnatal rubella. Isolation from child care or school should be recommended for 7 days after onset of rash. Intramuscular (IM) immunoglobulin (0.55 mL/kg) may reduce viral load and be beneficial for treating susceptible pregnant females who choose not to terminate pregnancy.3



Roseola is a typical viral rash with high-spiking fevers caused by human herpes virus 6 and 7 (HHV-6, HHV-7). The virus is transmitted through respiratory secretions from asymptomatic individuals and during the febrile viremic phase of the illness. Maternally transferred antibodies provide protection for the first 3 to 6 months of life. Therefore, it is typically seen in infants and toddlers between 6 months and 2 years of age. By the age of 4 years, virtually all children have serologic evidence of prior infection from HHV-6.


The classic presentation includes sudden onset of high fever to 40°C with fever spikes persisting for 72 hours followed by a transient erythematous maculopapular truncal rash that may progress to the extremities. From the time of exposure, the incubation period is approximately 9 to 10 days. The rash may occur up to 24 hours before or after the fever resolves and may be transient and escape detection. Infants with fever rarely appear ill and act remarkably well for the height of their fever. Large postoccipital lymph nodes are characteristic, and their presence in an infant with high fever can predict roseola as the cause of fever. A bulging fontanelle has been found in up to 25% of infants infected with HHV-6. If the infant is alert, playful, and without paradoxical irritability, meningitis is very unlikely.


Febrile convulsions have been seen in up to 20% to 30% of infants with roseola due to the height of fever and sudden rise in body temperature.7 Fatigue, irritability, and anorexia are reported occasionally. Pneumonia, aseptic meningitis, encephalitis, hepatitis, and hemophagocytic syndrome are rare, but have been reported in immunocompromised individuals.


Management is supportive, and fever may be treated for comfort. In severely immunosuppressed patients, IV ganciclovir may be considered.8 Although there is no prospective comparative data, the recommended dose is 10 to 20 mg/kg/d divided every 12 hours, given intravenously. The optimal length of treatment has not been reported.9



Erythema infectiosum is caused by the human parvovirus B19. Parvovirus is a single-stranded DNA unenveloped virus, with a tropism for erythroid progenitor cells. Humans are the only known host for carrying and transmitting the disease. Infection can occur at any age, but is most common in mid-to-late childhood. The virus is mainly transmitted through contact with respiratory secretions or from mother to fetus, but it can be carried through blood products.

Viremia occurs approximately 1 to 2 weeks after exposure and lasts 3 to 5 days. By the time the rash appears, most patients are no longer contagious. However, patients with hemolytic disease presenting with aplastic crises are shedding virus and can transmit disease to others up to 7 days after the rash appears.


The characteristic rash consists of bright erythema of the cheeks giving a “slapped cheek” appearance, and a fine, lacy, reticular rash on the extremities and trunk (Fig. 91-2).


FIGURE 91-2. Fifth disease. (Used with permission from Melissa Peters, MD)

The rash may resolve in a few days, only to reappear with exposure to sun or warm baths, and may recur for several weeks. Low-grade fever, arthralgia, headache, and myalgia may be seen in some children as a prodrome before the rash appears. Arthritis is rare in children, but common in adults.

Other presentations of infection with parvovirus B19 include the papulopurpuric glove-and-sock syndrome (Fig. 91-3). This consists of pruritic or painful petechiae and purpura limited to the hands and feet. Investigators have also isolated parvovirus B19 from occasional patients with Henoch–Schonlein purpura.


FIGURE 91-3. Papulopurpuric “glove and sock” syndrome. (Used with permission from Melissa Peters, MD)


The diagnosis is usually made by clinical observation, but antibody testing by radioimmunoassay or enzyme-linked immunosorbent assay may be used to identify presence of IgM during the acute phase of the illness. IgG antibody titer rise 2 to 3 weeks after the symptoms resolve. In the immunocompromised host, demonstration of the virus by PCR assay is preferred.


In a healthy host, complications are rare and limited to transient arthritis or arthralgias. Replication of virus in red cell precursors causes a transient reduction in red blood cell formation during the viremic phase. This is unimportant in an otherwise healthy child with a normal red cell survival of 120 days, but can cause serious symptoms when the normal red cell lifespan is short. Therefore, parvovirus causes major complications in three groups of patients—those with hemoglobinopathies or hemolytic anemia, immunocompromised patients, and the fetus.

Children with hemolytic disease and hemoglobinopathies (thalassemias, G6PD, iron deficiency, spherocytosis, sickle cell disease, and pyruvate kinase deficiency), and short red cell survival are at risk for aplastic crises with often critical drops in hemoglobin with no compensatory rise in reticulocyte counts during the viremic phase. These aplasias are generally self-limited and respond to red blood cell transfusions.10

Immunocompromised patients with HIV, acute leukemia, organ transplants, and lupus may have a more severe prolonged anemia because of chronic lysis. IVIG has been used successfully in some of these patients to shorten course of anemia.11

Pregnant women, especially during the first trimester are at risk for hydrops fetalis with extensive hemolysis, severe anemia, and high-output cardiac failure leading to generalized edema.


Supportive care is all that is necessary in healthy children. Patients with hemolytic anemia and aplastic crisis may require blood transfusions. For exposed pregnant women or those exhibiting classic symptoms, B19 IgM and IgG titers should be drawn, and if positive, those patients should be closely followed by ultrasound for signs of hydrops fetalis.



Varicella-zoster virus, a human herpes virus-3 (HHV-3), is the cause of both chicken pox and shingles. Widespread childhood immunization programs since 1995 have dramatically reduced the prevalence of varicella infection in children in the United States.

Humans are the only known reservoir for this highly contagious virus. The virus enters through the respiratory tract or conjunctivae, and is transferred from person-to-person by air or contact with fluid from vesicles. The incubation period is 10 to 21 days, and infected patients are most likely to be infectious to others from 2 days before the onset of rash until the lesions are crusted and dry.


A prodrome of nonspecific symptoms precedes the rash by 1 to 2 days. These can include nasal congestion, conjunctival injection, headache, malaise, anorexia, cough, and low-grade fever. The rash begins as erythematous macules that rapidly progress to papules and eventually form the characteristic vesicles on an erythematous base (dew drops on a rose petal). The rash is often pruritic and is found mainly on the head, trunk, and to a lesser extent, the extremities. Within 6 to 24 hours the vesicles become pustules that break and dry into crusts. New crops of lesions develop with all stages of lesions present on the skin at the same time. In a normal host the lesions resolve in 5 to 7 days (Fig. 91-4).


FIGURE 91-4. Varicella. (Used with permission from Melissa Peters, MD)


When confirmatory testing is necessary, PCR or direct fluorescent antibody of vesicles is preferred.


The most common minor complication is secondary bacterial infection of the skin lesions. Serious complications include varicella pneumonia, encephalitis, secondary bacterial pneumonia, cellulites, necrotizing fasciitis, and sepsis. The disease is more severe in adolescents and adults. Immunocompromised children and those on chronic corticosteroids are also at greater risk of these complications.

Congenital varicella syndrome with brain and eye anomalies, limb hypoplasia, and intrauterine growth retardation (IUGR) can occur in 0.4% to 2% of susceptible pregnant women who are infected during the first 20 weeks of gestation.12


Uncomplicated varicella in the normal host requires only symptomatic treatment to control itching. In healthy children, virus replication ends within 72 hours of onset of the rash, making late treatment with antiviral agents of no value. Starting acyclovir within the first 24 hours of rash development in low-risk children may modify the disease course.3 Oral acyclovir is indicated in moderate-risk children with chronic cutaneous or pulmonary disease, those on long-term salicylate therapy, children on short, intermittent oral or aerosol corticosteroids, and children older than the age of 12 years. For children who are at high risk of complications, specifically those on chronic corticosteroids and immunosuppressive agents, intravenous antiviral therapy should be started early. Intravenous immunoglobulin, or preferably, varicella-zoster immunoglobulin may modify the disease if given early after exposure.3 Please see Table 91-1 for antivirals and dosing guidelines. Varicella vaccine, when administered within 36 hours of exposure, can be useful in preventing disease and providing postexposure prophylaxis.13

TABLE 91-1

Antiviral Therapies3,9




Herpes zoster is a common complication of a prior varicella-zoster virus exposure with up to one million cases annually in the United States. As the primary varicella infection resolves, the virus remains latent in spinal sensory nerve root ganglia. Zoster is a reactivation of that latent virus. Herpes zoster is rare in children, but incidence increases with age and may have a lifetime incidence of 10% to 50%.

Lesions contain a high viral load and may be transmitted by airborne route. Patients are contagious from the time lesions first appear to when the last lesion has crusted over.


A prodrome of tingling pain may precede the onset of rash. Crops of vesicles occur, usually limited to a specific dermatome nerve distribution. Eruptions can occur anywhere, but are most commonly in a unilateral distribution over the thoracic or lumbosacral regions. The lesions start as crops of vesicles, but may burst and leave shallow ulcers that crust over with time (Fig. 91-5). In adolescents and adults, shingles can be extremely painful, but in children, pruritis rather than pain is often the chief complaint.


FIGURE 91-5. Herpes progenitalis in an infant. (Used with permission from Melissa Peters, MD)


Most often, diagnosis is made clinically. However, laboratory testing may be necessary in more atypical cases, in immunocompromised patients, and in cases of disseminated herpes zoster. Direct fluorescent antibody testing is rapid and specific, but is not very sensitive and depends on collection method. PCR is rapid and sensitive but may not be available in all circumstances. Tzanck staining can be done at the bedside but does no distinguish herpes zoster from herpes simplex virus (HSV). Serologic testing can be difficult. IgM can indicate primary infection or reactivation.14


Pain can persist for weeks to months, and may continue to recur without the presence of rash. Cranial nerves are rarely involved, but when present, corneal ulceration can be serious. If rash appears in this distribution, early ophthalmology involvement is essential. Post herpetic neuralgia is another common complication, resulting in persistent pain over the distribution area long after the rash has resolved.

Serious complications can occur in immunosuppressed patients and patients on chronic corticosteroids in the form of disseminated herpes zoster. This disseminated viremia can affect the intestines, liver, lungs, and brain causing an encephalitis, hepatitis, pneumonia, or sometimes disseminated intravascular coagulation (DIC). Without antiviral treatment disseminated visceral disease can have up to a 15% mortality rate.15


Treatment guidelines for management of shingles are the same as for chicken pox. Patients should be encouraged to keep rash clean and dry, and if possible, covered. They should avoid any topical antibiotics.

Famciclovir or valacyclovir are preferred for treatment of adults (Table 91-1).3 Steroids have been shown to decrease disease course but do not seem to have any effect on the development of postherpetic neuralgia (PHN). For symptomatic relief, nonsteroidal agents, acetaminophen, tricyclics, and opiates have been used with varying degrees of success. The US Food and Drug Administration has approved gabapentin and pregabalin in escalating doses for the treatment of PHN, although there are no studies to support use in children.16



Global prevalence of HSV increases with age affecting almost half of the population by the age of 15 years and 60% to 90% by adulthood. Clinical disease in humans is caused by two members of the Herpesviridae family, HSV1 and HSV2. The Herpes virus enters the host through epithelial cells and may undergo replication at the site of invasion. After the primary infection has occurred, HSV travels through the periaxonal sheath of sensory nerves to ganglia of the host nervous system. The cervical and lumbosacral sensory ganglia are particularly vulnerable. The virus replicates in ganglia and may persist for life. An asymptomatic person can shed virus, but during primary infection and reactivation, virus shedding is increased. Reactivation of virus can occur as a result of a variety of external and internal triggers including fever, immunosuppression, local trauma, menstruation, stress, fatigue, temperature changes, and exposure to sunlight.17


Clinical manifestations are highly variable and include primary and secondary presentations. Viral manifestation can result in encephalitis and serious systemic symptoms, self-limited simple mucocutaneous signs, or asymptomatic infection. HSV1 is mainly associated with infections involving the mouth, pharynx, and eyes, while HSV2 primarily shows genital mucosal symptoms. Overlap between types occurs, and both viruses enter the central nervous system and cause systemic disease by the same mechanism.

The most common manifestation of HSV1 is primary herpetic gingivostomatitis. This is seen in young children older than 6 months of age and may be subclinical. A prodrome of fever, irritability, malaise, and loss of appetite lasting 1 to 2 days is followed by vesicles on the oral mucosa and tongue that rapidly rupture and become superficial and painful ulcers. Perioral extension of the ulcers is common. An intense gingivitis is almost always present and helps to distinguish HSV from coxsackievirus enanthems. Tender submandibular adenopathy is usually present. Symptoms may last up to 2 weeks (see Chapter 97 for the review of genital HSV) (Fig. 91-6A).


FIGURE 91-6. Herpes simplex. (Used with permission from Melissa Peters, MD)

Another common presentation of HSV is recurrent orofacial herpes, commonly referred to as “fever blisters.” This secondary phenomenon occurs in 15% to 40% of patients who have had symptomatic or asymptomatic primary herpetic oral infections. Reactivation of virus decreases with age. There may be a prodrome of pain or pruritis before emergence of the labial ulcer. Less frequently, intraoral vesicles may recur.

A number of distinct secondary manifestations of HSV occur. Patches of cutaneous HSV occur commonly from contact of abraded skin with active oral or other herpes lesions actively shedding virus. Outbreaks among athletes have been termed “herpes gladiatorum.” Herpetic whitlow is caused by secondary inoculation of virus from mouth to fingers. This is common in children with primary herpetic gingivostomatitis who suck their thumbs or fingers (Fig. 91-6B). To the untrained eye, a whitlow can be confused with paronychia, and attempts at drainage can cause damaging cosmetic results. This is a self-limited problem with complete resolution in 2 to 3 weeks.

Eczema herpeticum (Kaposi varicelliform eruption) is an uncommon but serious primary manifestation of HSV in children with atopic dermatitis and breaks in skin integrity. The virus is usually transmitted from a labial lesion on the caregiver to the eczematous eruption (Fig. 91-6C). Erythema multiforme (EM) has been associated with HSV reactivation and possibly with primary infections. In some series, presence of HSV with EM has been as high as 75%.18 Recurrent EM with recrudescence of HSV can occur repeatedly with attacks lasting up to 2 weeks. The characteristic acral EM rash (erythematous and of multiforme) occurs within 10 days of reactivation and may last 2 weeks (see Chapter 86).

In the US, neonatal herpes occurs in up to 0.15% of births.19 Most infections arise from intrapartum transfer of virus, but can be contracted postnatally from oral, genital, or hand contact from a caregiver or from contaminated fomites. Three distinct clinical entities can result. Disseminated herpes presents in the first 1 to 4 weeks of life with a clinical presentation similar to bacterial sepsis and a mortality rate of 25% with antiviral treatment. Symptoms may occur as late as 6 weeks of life. Herpes encephalitis may present with seizures in the neonatal period and, if untreated, will progress to systemic disease. Neonatal herpes with involvement limited to the skin, eye, and mouth can result in minimal morbidity if treated early with antiviral agents. Congenital HSV infection is rare, but presents as a small for gestational-age infant, usually premature, and with microcephaly, retinitis, and vesicular rash.


Uncomplicated HSV infection can be diagnosed clinically. When necessary, DFA of skin lesions provides quick and reliable results. PCR of the cerebrospinal fluid is particularly useful in diagnosing neonatal HSV and herpes encephalitis. Use of the Tzanck smear for diagnosis should be discouraged. There is a high incidence of false-negatives, and the Tzanck test cannot distinguish HSV from varicella-zoster virus. Culture from lesions or body fluids will grow in vitro in 1 to 15 days.


Serious complications are mainly limited to the immunocompromised host, the neonate, and those with involvement of the eye or central nervous system. Ocular herpes or herpes keratoconjunctivitis remains a major cause of blindness worldwide. Conjunctivitis can be unilateral or bilateral and result in corneal ulcerations. Herpes meningoencephalitis may occur at any age and have no skin manifestations at presentation. Neonatal herpes in the first 6 weeks of life, as described above has significant mortality and morbidity even with adequate treatment. Scarring is uncommon, but can occur, especially with eczema herpeticum in children with chronic cutaneous conditions.


Antiviral agents can suppress virus replication and modify the clinical course but cannot eradicate the virus. Acyclovir is the mainstay for systemic disease in neonates, infants, and young children. However, its poor bioavailability and short plasma half-life make newer but more expensive options attractive for treatment of adolescents and immunosuppressed hosts. These include drugs with greater bioavailability such as valacyclovir and famciclovir. (Table 91-1)

Topical antiviral agents such as docosanol 10%, penciclovir 1%, and acyclovir 5% creams have been shown to reduce the symptoms of recurrent labial herpes when started early during the prodrome. Careful monitoring for bacterial super infection is important as well, and should be addressed as it occurs.



The enterovirus group, including echovirus and coxsackievirus, consists of nearly 80 human host infections that may cause childhood exanthems. Although they rarely cause serious or life-threatening disease, some enterovirus infections can result in serious sequelae such as encephalitis, myocarditis, and septic shock.20


Although most enteroviral infections have nonspecific clinical presentations, a few are associated with clinically distinguishable exanthems and/or enanthems.

Hand–foot–mouth syndrome is associated with infection from coxsackievirus A16 and enterovirus 71. A brief prodrome of low fever, malaise, and abdominal pain that may precede the skin and mucosal manifestations by 1 to 2 days. Orally, vesicles appear most commonly on the tongue, hard palate, and buccal mucosa lasting 5 to 7 days. Small vesicles appear shortly after oral lesions on the sides of fingers, palms, and soles, and quickly rupture leaving fine erythematous macules. The skin lesions occasionally may be found on the buttocks and trunk. The symptoms resolve in less than a week in a normal host. Treatment is aimed at symptomatic improvement of oral pain with topical lidocaine and mouthwashes (Fig. 91-7).


FIGURE 91-7. Hand–foot–mouth disease. (Used with permission from Melissa Peters, MD)

Complications are rare, with most cases benign and self-limited, but myocarditis, pneumonia, flaccid paralysis, pulmonary edema, and meningoencephalitis have been reported. In the last decade, several epidemics, mostly in Southeast Asia, have been caused by enterovirus 71 with reported complications of neurogenic pulmonary edema, shock, and rhomboencephalitis which can be acutely fatal. The CDC reports that those with complications of meningoencephalitis and pulmonary edema were more likely to present with myoclonic jerks, fever lasting >3 days, lethargy, or prolonged temperatures >39°C, and should be evaluated more closely. Therefore, although normally a self-limited disease, patients with hand–foot–mouth disease should be evaluated with careful history and physical.2123

Herpangina is another characteristic enanthem caused by coxsackievirus A1 to A8 and A12. Examination of the oropharynx reveals small erythematous vesicles localized to the soft palate and anterior tonsillar fossae. This is mainly a disease of infants and toddlers with refusal to eat, low-grade fever, and irritability as the presenting symptoms. Diagnosis is made by clinical examination and needs no further testing. Treatment is symptomatic to prevent dehydration and lesions usually resolve in 5 to 7 days.


Management of enteroviral infection consists mainly of supportive care. In patients with oral lesions, focus is often on hydration in young children refusing to drink fluids. Some may need admission for pain control and IV fluids.



Pityriasis rosea is a benign, self-limited exanthem that does appear in clusters, but there is no evidence of person-to-person spread and the cause is unknown. HHV-6 and HHV-7 have been proposed as viral triggers, but it has never been proved. In children, it occurs most commonly in adolescents and young adults. Clinical presentation starts with the “herald patch,” an oval, scaly, 2- to 5-cm lesion that is often confused with a fungal dermatitis, and occurs 1 to 20 days before onset of a generalized rash. This is followed by multiple rose-pink ovoid macules that have a “Christmas tree” distribution over the back following Langerhans lines. It may also involve the trunk and extremities to a lesser degree. The face is usually spared. The rash lasts 2 to 6 weeks and may be associated with no symptoms or low-grade fever, headache, malaise, nausea, and pruritis.

Treatment is generally symptomatic. After the acute inflammatory stage has passed, ultraviolet B (UVB) may be used to speed involution of the lesions. Topical emollients, steroids, and oral antihistamines may be used to treat associated pruritus, which is often intense. The rash resolves untreated without sequelae or scarring (Fig. 91-8).


FIGURE 91-8. Pityriasis. (Used with permission from Melissa Peters, MD)


Molluscum contagiosum is a common skin rash now known to be caused by the molluscum contagiosum virus. The rash is characterized by flesh-colored or pink “pearly papules” that are often umbilicated. Lesions begin as discreet firm, small dome-shaped growths with a waxy or pearly surface. The rash is usually painless, but may be pruritic, especially in children (Fig. 91-9).


FIGURE 91-9. Molluscum contagiosum. (Used with permission from Melissa Peters, MD)

Molluscum is spread by direct skin contact, towels, or clothing. Patients continue to spread virus and remain contagious until the rash completely clears. Most patients only have 10 to 20papules. However, a patient with a weakened immune system may have hundreds of papules.

Most molluscum rashes resolve in 3 to 6 months without treatment and do not scar. If the rash is on the face, the patient is immunosuppressed, or if it is affecting quality of life, referral to a dermatologist is appropriate. The rash can be treated by topical therapies prescribed by curettage laser therapy to accelerate resolution. Complications are rare. Molluscum of the eyelid is rare but could affect vision and should be referred to a dermatologist. If a patient has a more severe case of molluscum, immunodeficiency should be considered.24


First described in 1955 and originally termed papular acrodermatitis of childhood, this rash consists of discrete, nonpruritic, erythematous, monomorphic papules, and occasionally vesicles on the face, buttocks, and extensor surfaces of the extremities. It usually spares the trunk. Patients may have a prodrome of nonspecific upper respiratory symptoms, and may have associated lymphadenopathy, hepatomegaly, or splenomegaly. The rash usually resolves in 2 to 3 weeks, although it may last up to 8 weeks. Originally thought to be associated with hepatitis B, it has since been described in association with EBV, measles, coxsackievirus A16, CMV, parainfluenza, and influenza among others. Care is supportive and patient should undergo lab evaluation if anything in history of physical suggests hepatitis20(Fig. 91-10).


FIGURE 91-10. Gianotii–Crosti syndrome. (Used with permission from Melissa Peters, MD)


1. World Health Organization. Measles Accessed November 11, 2012.

2. Center for Disease Control. Measles Serology. Accessed November 3, 2012.

3. American Academy of Pediatrics. In: Pickering LK, ed. Red Book: 2012 Report of the Committee on Infectious Diseases. 29th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2012.

4. Semba RD, Bloem MW. Measles blindness. Surv Ophthalmol. 2004;49(2):243–255.

5. Center for Disease Control. Manual for the Surveillance of Vaccine-Preventable Diseases. Rubella. (5th ed. 2012) Accessed November 11, 2012.

6. Rubella. The Pink Book: Epidemiology and Prevention of Vaccine Preventable Diseases. 12th ed. Second Printing (May 2012).

7. Millichap JG, Millichap JJ. Role of viral infections in the etiology of febrile seizures. Pediatr Neurol. 2006;35(3):165–172.

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