Most childhood exanthems are benign, self-limited, and require no treatment; however, they can be associated with myocarditis, encephalitis, or pneumonia.
Worldwide, rubeola is still a major cause of morbidity and mortality. Early recognition can control spread. Increase in rates of nonmedical vaccine exemptions have been associated with an increase in disease rates in the United States.
Roseola infantum is a common cause of febrile seizures in infants. A full fontanelle may be present in up to 25%.
Children with varicella who 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 and being familiar with the history and physical findings associated with these specific exanthems can be crucial to reassuring and educating families, 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 describes recognizable childhood exanthems, discusses risks of exposure, and describes 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. However, widespread use of live virus vaccine during the past 40 years has dramatically reduced the incidence of the disease in developed countries; the rates of parental refusal of immunizations due to nonmedical exemptions (either the parent feels the immunizations conflict with their religious or spiritual beliefs, or they object to the immunization for moral or philosophical reasons) have increased steadily in the past 20 years. Maternally acquired antibodies usually are sufficient to protect against clinical exposure in infants younger than 1 year of age. In the United States, the American Academy of Pediatrics (AAP) recommends measles, mumps, rubella (MMR) vaccination between 12 and 15 months of age, and a second dose at 5 years. In the most recent measles outbreak in the United States in 2014, approximately half of the cases were patients who were vaccine eligible but unvaccinated.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. 92-1A) 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.
The rash is a maculopapular erythematous rash that first appears on the face and then 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. 92-1B). 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 have been 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 the 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 herpesvirus 6 and 7 (HHV-6, HHV-7), members of the human cytomegalovirus family. 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. There have also been some reports of primary infection or reactivation of HHV-6 infection being associated with development of temporal lobe epilepsy.
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. 92-2).
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 (PPGSS) (Fig. 92-3). This presentation is more common in adults and consists of pruritic or painful petechiae and purpura limited to the hands and feet. This can sometimes be associated with mucosal involvement as well. Investigators have also isolated parvovirus B19 from occasional patients with Henoch–Schönlein purpura.
In addition to the dermatologic manifestations, parvovirus B19 can also cause acute arthropathy, more commonly in adolescents and adults. In children, the arthropathy most commonly affects larger joints, particularly knees and ankles.
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 titers rise 2 to 3 weeks after the symptoms resolve. In the immunocompromised host, demonstration of the virus by PCR assay is preferred.
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