Transmission and Risk.

Measles (rubeola or morbilli) is a highly contagious viral disease transmitted by contact with droplets from infected individuals ( Box 14.1 ). The virus is spread by coughing and sneezing, close personal contact, or direct contact with infected nasal or throat secretions. The virus remains active and contagious in the air or on infected surfaces for up to 2 hours. It can be transmitted by an infected individual from 4 days before the onset of the rash to 4 days after the onset. If one person has the disease, a high proportion of their susceptible close contacts will also become infected. Unimmunized young children are at highest risk for measles and its complications, including death. Measles can be particularly deadly in countries experiencing or recovering from war, civil strife, or a natural disaster. Infection rates soar because damage to health services interrupts routine immunization. Overcrowding in camps for refugees and internally displaced people greatly increases the risk of infection.

Complications.

Most cases have a benign course.

Severe measles is likely in poorly nourished young children, especially if they do not receive sufficient vitamin A, or are immunocompromised by human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) or other diseases.

Children die from complications. Complications are more common in children younger than age 5 years or adults older than age 20 years. The most serious complications include blindness, encephalitis, severe diarrhea, and ear infections. Pneumonia is the most common cause of death associated with measles. Encephalitis occurs in 1 out of 1000 cases; otitis media is reported in 5% to 15% of cases and pneumonia in 5% to 10% of cases. Survivors of encephalitis often have permanent brain damage and subsequent mental disability. The case death rate in developing countries is 1% to 5%, but may be as high as 25% in populations where high levels of malnutrition and poor access to health care exist. People who recover from measles are immune for life. Measles occurring during pregnancy may affect the fetus. Most commonly, this involves premature labor and moderately increased rates of spontaneous abortion and low-birth-weight infants. Measles infection in the first trimester of pregnancy may be associated with an increased rate of congenital malformation.

Incidence.

Measles continues to be a major health concern in many parts of the world, including select countries in Africa, Asia, the Pacific and Europe ( Fig. 14.1 ). The World Health Organization (WHO) estimates that between 2000 and 2017, measles vaccination prevented 21.1 million deaths, which represents an 80% reduction from previous years. In 2017, 110,000 people died from measles; most were under the age of 5. In the United States, large measles outbreaks occur when travelers return to the United States infected with measles. Most people who become infected with measles are not immunized. In 2014, the United States experienced the largest number of reported cases (667 cases from 27 states), since measles was eliminated from the United States in 2000. Communities at greatest risk are those with high numbers of unimmunized individuals (e.g., Amish communities), highlighting the importance of immunizing children.

Measles incidence rate per million (12-month period). Based on data received 2018-02 and covering the period between 2017-01 and 2017-12. Incidence: number of cases/population** 100,000.

*World population prospects, 2017 revision.

**Countries with the highest number of cases for the period.

***Countries with the highest incidence rates (excluding those already listed in the table above).

From World Health Organization.

Vaccine.

The recommended age of first vaccination varies from 6 to 15 months and is a balance between the optimum age for seroconversion and the probability of acquiring measles before that age. The proportions of children who develop protective concentrations of antibody after measles vaccination are about 85% at age 9 months and 95% at 12 months. Two doses of measles vaccine are needed to achieve sufficiently high levels of population immunity to interrupt transmission. WHO recommends that the first dose of measles vaccine be administered at age 9 months, although countries in which the risk of measles is low often provide the first dose at age 12 to 15 months. The duration of vaccine-induced immunity is at least several decades. Secondary vaccine failure rates are estimated to be about 5% at 10 to 15 years after immunization, but are probably lower when vaccination is given after 12 months of age. Decreasing antibody concentrations do not necessarily imply a complete loss of protective immunity, because a secondary immune response usually develops after re-exposure to measles virus, with a rapid rise in antibody titers without overt clinical disease. Fever to 39.4° C (103° F) occurs in about 5% of seronegative vaccine recipients.

Laboratory Confirmation.

The detection of measles virus–specific immunoglobulin M (IgM) in a specimen of serum or oral fluid is diagnostic of acute infection and is the most commonly used serologic test. Acute infection can be confirmed with a four times or greater increase in measles virus–specific IgG antibody concentrations between acute and convalescent sera. The presence of IgG antibodies to measles virus in a single serum specimen is evidence of previous infection or immunization, which cannot be distinguished serologically. Measles virus–specific IgM antibodies might not be detectable until 4 days or more after rash onset and usually fall to undetectable concentrations within 4 to 8 weeks of rash onset. Measles RNA by real-time polymerase chain reaction (RT-PCR) also confirms measles infection.

Eruptive Phase.

The rash begins on the fourth or fifth day on the face and behind the ears, but in 24 to 36 hours it spreads to the trunk and extremities ( Fig. 14.3 ). It reaches maximum intensity simultaneously in all areas in approximately 3 days and fades after 5 to 10 days. The rash consists of slightly elevated maculopapules that vary in size from 0.1 to 1.0 cm and vary in color from dark red to a purplish hue. They are frequently confluent on both the face and the body, a feature that is such a distinct characteristic of measles that eruptions of similar appearance in other diseases are termed morbilliform (looks like measles). The early rash blanches on pressure; the fading rash is yellowish brown with a fine scale, and it does not blanch. Supportive treatment is the only necessity unless complications, such as bacterial infection or encephalitis, appear.

Measles – progression of disease. A, Koplik spots appear as red spots with bluish white centers, “grains of sand.” They may occur anywhere in the mouth. B, A maculopapular rash appears on the face and becomes confluent. C, The rash then appears on the trunk.

Vitamin A Treatment.

Vitamin A, retinol-binding protein (RBP), and albumin levels are significantly reduced early in the exanthem. Treatment with vitamin A reduces morbidity and mortality in measles, and all children with severe measles should be given vitamin A supplements regardless of whether they are thought to have a nutritional deficiency.

This can help prevent eye damage and blindness. Vitamin A–treated children recover more rapidly from pneumonia and diarrhea, have less croup, and spend fewer days in the hospital. Treated patients have an increase in the total number of lymphocytes and measles IgG antibody. Also, for treated patients the risk of death or a major complication during a hospital stay is half that of untreated patients.

WHO recommends administration of once-daily doses of 200,000 international units of vitamin A for 2 consecutive days to all children aged 12 months or older who have measles.

Lower doses are recommended for younger children: 100,000 international units per day for children aged 6 to 12 months and 50,000 international units per day for children younger than 6 months. In children with clinical evidence of vitamin A deficiency, a third dose is recommended 2 to 4 weeks later.

Immunity.

Persons are considered immune if they have written documentation of adequate immunization with live measles vaccine on or after the first birthday, physician-diagnosed measles, or laboratory evidence of measles immunity. Most persons born before 1957 are likely to have been naturally infected and generally need not be considered susceptible. Routine serologic screening to determine measles immunity is not recommended.

Individuals Exposed to Disease.

Live vaccine, if given within 72 hours of measles exposure, may provide protection and is preferable to the use of human immunoglobulin in persons at least 12 months of age if there is no contraindication.

Revaccination Risks.

There is no enhanced risk from administering live measles vaccine to persons who are already immune to measles.

Pregnancy.

Live measles vaccine should not be given to women known to be pregnant or who are considering becoming pregnant within 3 months after vaccination. This precaution is based on the theoretical risk of fetal infection.

Clinical Presentation.

The incubation period is 4 to 6 days. There may be mild symptoms of low-grade fever, sore throat, and malaise for 1 or 2 days. Twenty percent of patients develop submandibular and/or cervical lymphadenopathy.

Eruptive Phase.

Oral lesions, present in 90% of cases, are generally the initial sign ( Fig. 14.4 ). Aphthae-like erosions varying from a few to 10 or more appear anywhere in the oral cavity and are most frequently small and asymptomatic. The cutaneous lesions, which occur in approximately two thirds of patients, appear less than 24 hours after the enanthem. They begin as 3- to 7-mm, red macules that rapidly become pale, white, oval vesicles with a red areola. There may be a few inconspicuous lesions, or there may be dozens. The vesicles occur on the palms, soles ( Figs. 14.5 to 14.7 ), dorsal aspects of the fingers and toes, and occasionally on the face, buttocks, and legs. They heal in approximately 7 days, usually without crusting or scarring. Nail matrix arrest was reported in a small group of children after HFMD. Beau lines (transverse ridging) and/or onychomadesis (nail shedding) followed HFMD by 3 to 8 weeks.

Hand-foot-and-mouth disease. Aphthae-like erosions may appear anywhere in the oral cavity.

Hand-foot-and-mouth disease. A cluster on the hand and sole of a young boy.

Hand-foot-and-mouth disease. The pale, white, oval vesicles with a red areola are a distinguishing feature of this disease.

Hand-foot-and-mouth disease. Cloudy vesicles with a red halo are highly characteristic of this disease.

Serious and Fatal Cases.

Although most cases of HFMD do not result in serious complications, outbreaks of HFMD caused by EV71 can present with a high rate of neurologic complications, including meningoencephalitis, pulmonary complications, and possibly death. HFMD caused by EV71 has become a major emerging infectious disease in Asia.

Differential Diagnosis.

When cutaneous lesions are absent, the disease may be confused with aphthous stomatitis. The oral erosions of HFMD are usually smaller and more uniform. The vesicles of herpes appear in clusters, and those of varicella endure longer and always crust. Both varicella and herpes have multinucleated, giant cells in smears taken from the moist skin exposed when a vesicle is removed (Tzanck smear). Giant cells are not present in lesions of HFMD. Eczema herpeticum, due to herpes simplex virus, may be differentiated from eczema coxsackium with a herpes simplex viral culture or PCR.

Treatment.

Symptomatic relief and reassurance are all that are required.

Incubation Period.

The incubation period of scarlet fever ( Fig. 14.8 ) is 2 to 4 days.

Scarlet fever. Evolution of signs and symptoms.

Prodromal and Eruptive Phase.

The sudden onset of fever and pharyngitis is followed shortly by nausea, vomiting, headache, and abdominal pain. The entire oral cavity may be red, and the tongue is covered with a yellowish white coat through which red papillae protrude. Diffuse lymphadenopathy may appear just before the onset of the eruption. The systemic symptoms continue until the fever subsides. The rash begins around the neck and face and spreads in 48 hours to the trunk and extremities; the palms and soles are spared ( Fig. 14.9 ). The face is flushed except for circumoral pallor, whereas all other involved areas exhibit a vivid scarlet hue with innumerable pinpoint papules that give a sandpaper quality to the skin ( Fig. 14.10 ). The rash is more limited and less dramatic in milder cases. Linear petechiae (Pastia sign) are characteristic; they are found in skin folds, particularly the antecubital fossa and inguinal area. The tongue sheds the white coat to reveal a red, raw, glazed surface with engorged papillae ( Fig. 14.11 ).

Scarlet fever. Early eruptive stage on the trunk showing numerous pinpoint red papules.

Scarlet fever. Fully evolved eruption. Numerous papules giving a sandpaper-like texture to the skin.

Scarlet fever. Portions of the white coat remain in the center, but the remainder of the tongue is red with engorged papillae (“strawberry tongue”).

The fever and rash subside and desquamation appears, more pronounced than in any of the eruptive fevers. It begins on the face, where it is sparse and superficial; progresses to the trunk, often with a circular, punched-out appearance; and finally spreads to the hands ( Fig. 14.12 ) and feet ( Figs. 14.13 and 14.14 ), where the epidermis is the thickest. Clinically, the hands and feet appear normal during the initial stages of the disease. Large sheaths of epidermis may be shed from the palms and soles in a glove-like cast, exposing new and often tender epidermis beneath. A transverse groove may be produced in all of the nails (Beau lines) ( Fig. 14.15 ). The pattern of desquamation of the palms and soles and grooving of the nails is such a distinct characteristic of scarlet fever that it is helpful in making a retrospective diagnosis in cases where the eruption is minimal. A rising antistreptolysin-O titer constitutes additional supporting evidence for a recent infection. Desquamation is generally complete in 4 weeks, but it may last for 8 weeks. Recurrence rates of scarlet fever as high as 18% have been reported.

Scarlet fever. Desquamation of the hands begins 7 to 10 days after resolution of the rash. Peeling occurs in the axillae, on the groin, and on the tips of the fingers.

Scarlet fever. Desquamation of the feet.

Scarlet fever. Desquamation of the feet.

Scarlet fever. Beau lines: transverse grooves on all nails several weeks after skin signs of scarlet fever have cleared.

Treatment.

Treat with penicillin, amoxicillin, cephalosporin such as cephalexin or cefadroxil, clindamycin, azithromycin and clarithromycin ( Table 14.2 ).

Congenital Rubella Syndrome.

Women who become infected with rubella early in the first trimester of pregnancy may transmit the virus to the fetus, resulting in a number of congenital defects (congenital rubella syndrome).

Incubation Period.

The incubation period of rubella ( Fig. 14.16 ) is 18 days, with a range of 14 to 21 days.

Rubella. Evolution of signs and symptoms.

Prodromal Phase.

Mild symptoms of malaise, headache, and moderate temperature elevation may precede the eruption by a few hours or a day. Children are usually asymptomatic. Lymphadenopathy, characteristically postauricular, suboccipital, and cervical, may appear 4 to 7 days before the rash and be maximal at the onset of the exanthem. In 2% of cases, petechiae on the soft palate occur late in the prodromal phase or early in the eruptive phase.

Eruptive Phase.

The eruption begins on the neck or face and spreads in hours to the trunk and extremities ( Fig. 14.17 ). The lesions are pinpoint to 1 cm, round or oval, pinkish or rosy red macules or maculopapules. The color is less vivid than that of scarlet fever and lacks the blue or violaceous tinge seen in measles. The lesions are usually discrete but may be grouped or coalesced on the face or trunk. The rash fades in 24 to 48 hours in the same order in which it appeared and may be followed by a fine desquamation.

Rubella. The rash begins as macules on the face that spread to the trunk and the extremities. The macules may coalesce on the trunk.

Among adults infected with rubella, transient polyarthralgia or polyarthritis occurs frequently. These manifestations are particularly common among women.

Arthritis, affecting primarily the phalangeal joints of women, may occur in the prodromal period and may last for 2 to 3 weeks after the rash has disappeared. No treatment is required.

Central nervous system (CNS) complications (e.g., encephalitis) occur at a ratio of 1 : 6000 cases and are more likely to affect adults. Thrombocytopenia occurs at a ratio of 1 : 3000 cases and is more likely to affect children.

Serologic Testing.

Rubella IgG is often used as a marker of past infection or response to vaccination. This test is especially important in women of child-bearing age and is included in the recommended prenatal blood tests. The presence of IgG typically indicates immunity to acute rubella infection. Diagnosis is made on clinical findings as well as specific rubella IgM or a significant rise in rubella IgG titers in acute and convalescent serum specimens. RT-PCR and viral culture are other methods to detect rubella infection. Rubella is a reportable disease in the United States.

Vaccine.

The rubella vaccine is a live attenuated virus. Although it is available as a single preparation, it is recommended that in most cases rubella vaccine be given as part of the MMR vaccine. MMR is recommended at 12 to 15 months (not earlier) and a second dose when the child is 4 to 6 years old (before kindergarten or first grade). Rubella vaccination is important for nonimmune women who may become pregnant because of the risk for serious birth defects if they acquire the disease during pregnancy.

Erythema Infectiosum (Acute B19 Viral Infection).

Erythema infectiosum (fifth disease) is caused by the B19 parvovirus. It is relatively common and mildly contagious and appears sporadically or in epidemics, especially in the winter and spring. Peak attack rates occur in children between 5 and 14 years of age. Asymptomatic infection is common.

Infection causes erythema infectiosum in immunocompetent patients. It is the primary cause of transient aplastic crisis in patients with underlying hemolytic disorders. Persistent infection in immunosuppressed patients may present as red cell aplasia and chronic anemia. In utero infection may result in hydrops fetalis or congenital anemia. There is no evidence of reinfection in immunocompetent individuals.

Seroprevalence is 2% to 10% in children younger than 5 years, 40% to 60% in adults older than 20 years, and 85% or more in those older than 70 years. The average annual seroconversion rate of women of child-bearing age is 1.5%.

The virus may be transmitted via the respiratory route and via the transfusion of infected blood and blood products. Nosocomial transmission has been well documented. Individuals are not viremic or infectious at the rash or arthropathy stage of disease.

Incubation Period.

The incubation period of erythema infectiosum ( Fig. 14.18 ) is 13 to 18 days. Viremia occurs after the incubation period and reticulocyte numbers fall, resulting in a temporary drop in hemoglobin concentration of 1 g/dL in a normal person.

Erythema infectiosum. Evolution of signs and symptoms.

There is a nonspecific prodromal illness, followed by a three-stage erythematous disease.

Prodromal Symptoms.

Symptoms are usually mild or absent. Pruritus, low-grade fever, malaise, and sore throat precede the eruption in approximately 10% of cases. Lymphadenopathy is absent. Older individuals may complain of joint pain.

Eruptive Phase.

There are three distinct, overlapping stages.

Facial Erythema (“Slapped Cheek”).

Red papules on the cheeks rapidly coalesce in hours, forming fiery red, slightly edematous, warm, erysipelas-like plaques that are symmetric on both cheeks and spare the nasolabial fold and the circumoral region ( Fig. 14.19 ). The “slapped cheek” appearance fades in 4 days. The classic “slapped cheek” is much more common in children than in adults.

Erythema infectiosum. Facial erythema “slapped cheek.” The red plaque covers the cheek and spares the nasolabial fold and the circumoral region.

Net Pattern Erythema.

This unique characteristic eruption – erythema in a fishnet-like pattern – begins on the extremities approximately 2 days after the onset of facial erythema and extends to the trunk and buttocks, fading in 6 to 14 days ( Fig. 14.20 ). At times, the exanthem begins with erythema and does not become characteristic until irregular clearing takes place. This second-stage rash may vary from very faint erythema to a florid exanthem. Livedo reticularis has a similar net-like pattern, but it does not fade quickly.

Erythema infectiosum. A, A macular eruption appears on the extensor extremities. B, The eruption fades into a lacy net-like pattern.

Recurrent Phase.

The eruption may fade and then reappear in previously affected sites on the face and body during the next 2 to 3 weeks. Temperature changes, emotional upsets, and sunlight exposure may stimulate recurrences. The rash fades without scaling or pigmentation. There may be a slight lymphocytosis or eosinophilia.

Polyarthropathy Syndrome and Pruritus

Infection in the Pregnant Woman (Intrauterine Infection and Spontaneous Abortion).

In pregnant women, infection can, but usually does not, lead to fetal infection ( Box 14.2 ). Fetal infection sometimes causes severe anemia, congestive heart failure, generalized edema (fetal hydrops), and death. Many fetuses dying because of this infection are not noticeably hydropic.

Parvovirus B19 probably causes 10% to 15% of all cases of nonimmune hydrops. If the fetus survives fetal hydrops caused by B19, there usually are no long-term sequelae.

The fetus has a high rate of red cell production; its immature immune system may not be able to mount an adequate immune response. Parvovirus has been implicated as a cause of spontaneous abortion (from severe fetal anemia and hydrops fetalis).

Maternal infection in the first half of pregnancy is associated with 10% excess fetal loss and hydrops fetalis in 3% of cases (of which up to 60% resolve spontaneously or with appropriate management). B19-associated congenital abnormalities have not been reported among several hundred live-born infants of B19-infected mothers. The overall risk of serious adverse outcome from occupational exposure to parvovirus B19 infection during pregnancy is low (excess early fetal loss in 2 to 6 of 1000 pregnancies and fetal death from hydrops in 2 to 5 of 10,000 pregnancies). It is not recommended that susceptible pregnant women be excluded routinely from working with children during epidemics.

The polymerase chain reaction is a sensitive and rapid method for the diagnosis of intrauterine infection.

Anemia.

The virus has the propensity to infect and lyse erythroid precursor cells and interrupt normal red cell production. In a person with normal hematopoiesis, B19 infection produces a self-limited red cell aplasia that is clinically unapparent. In patients who have increased rates of red cell destruction or loss and who depend on compensatory increases in red cell production to maintain stable red cell indices, B19 infection may lead to transient aplastic crisis. Patients at risk for transient aplastic crisis include those with hemoglobinopathies (sickle cell disease, thalassemia, hereditary spherocytosis, and pyruvate kinase deficiency) and those with anemias associated with acute or chronic blood loss. B19 infection accounts for most, if not all, aplastic crises in sickle cell disease, but at least 20% of infections do not result in aplasia. Up to 30% of hospital staff members may be infected when exposed to infected sickle cell patients. In immunodeficient persons and those with AIDS, B19 may persist, causing chronic red cell aplasia, which results in chronic anemia. Some of these patients may be cured with immune globulin therapy.

Laboratory Evaluation.

Most acute infections with B19 are diagnosed in the laboratory by serologically detecting IgG and IgM class antibodies with enzyme immunoassay. IgM antibodies are the most sensitive indicator of acute B19 infection in immunologically normal persons. Measuring IgM level is useful for diagnosing recent parvovirus infection. Both IgG and IgM may be present at or soon after onset of illness and reach peak titers within 30 days. Because IgG antibody may persist for years, diagnosis of acute infection is made by the detection of IgM antibodies, unless one can demonstrate a 4-fold rise in IgG in acute and convalescent titers. The prevalence of parvovirus B19 IgG antibodies increases with age. The age-specific prevalence of antibodies to parvovirus is 2% to 9% of children younger than 5 years, 15% to 35% in children 5 to 18 years of age, and 30% to 60% in adults (19 years or older). IgM is detectable for as long as 3 months after exposure. Parvovirus B19 can be detected in blood, amniotic fluid, and synovial fluid by rapid PCR.

Management.

Most health departments do not recommend exclusion from school for children with fifth disease. Many infections are unapparent, and exposure may occur in the community, as well as in school.

Evaluate the immune status of exposed pregnant women. The risks are nil if the women is IgG positive. If she is not immune (although the risk of the fetus being affected is very low), fetal surveillance by repeated ultrasonographic examination and immune status reevaluation is recommended.

Because the major immune response appears to be humoral, patients with chronic infection have been treated with immune globulin. These patients often respond with a marked reduction in the level of B19 viremia and with reticulocytosis, followed within a few weeks by resolution of the anemia. Patients with persistent infection should be monitored for evidence of relapse by observation of the reticulocyte counts and by assays for B19 viremia when indicated.

Incubation Period.

The incubation period of roseola infantum ( Fig. 14.21 ) is 12 days, with a range of 5 to 15 days.

Roseola infantum. Evolution of signs and symptoms.

Prodromal Symptoms.

There is a sudden onset of high fever of 103° F to 106° F, with few or minor symptoms. Most children appear inappropriately well for the degree of temperature elevation, but they may experience slight anorexia or one or two episodes of vomiting, running nose, cough, and hepatomegaly. Seizures (but more frequently general cerebral irritability) may occur before the eruptive phase. Most recover without sequelae. Cases of encephalitis/encephalopathy with abnormal electroencephalograms and cerebral computed tomograms have been reported; epilepsy developed in one case and in another case the patient died. HHV-6 DNA has been detected in the cerebrospinal fluid (CSF); this suggests that HHV-6 may invade the brain during the acute phase. HHV-6 infection should be suspected in infants with febrile convulsions, even those without the exanthem. Mild to moderate lymphadenopathy, usually in the occipital regions, begins at the onset of the febrile period and persists until after the eruption has subsided.

Eruptive Phase.

The rash begins as the fever subsides. The term exanthema subitum indicates the sudden “surprise” of the blossoming rash after the fall of the fever. Numerous pale pink, almond-shaped macules appear on the trunk and neck, become confluent, and then fade in a few hours to 2 days without scaling or pigmentation ( Figs. 14.22 and 14.23 ). The exanthem may resemble rubella or measles, but the pattern of development, distribution, and associated symptoms of these other exanthematous diseases are different.

Roseola. Numerous pale pink, almond-shaped macules.

Roseola. Pale pink macules may appear first on the neck.

Laboratory Evaluation.

Leukocytosis develops at the onset of fever, but leukopenia with a neutropenia and relative lymphocytosis appears as the temperature increases and persists until the eruption fades. Seroconversion during the convalescent phase can be detected with immunofluorescence or enzyme immunoassays. HHV-6 can be detected by rapid PCR.

Treatment.

Control the patient’s temperature with aspirin and provide reassurance. HHV-6 is inhibited by several antiviral drugs in the laboratory, including ganciclovir and foscarnet. Treatment may be considered for patients with serious HHV-6-associated disease confirmed with virologic tests.

Systemic Symptoms.

Many are possible, such as fever, nausea, vomiting, and diarrhea, along with typical viral symptoms of photophobia, lymphadenopathy, sore throat, and possibly encephalitis.

Exanthem.

The rash may appear at any time during the course of the illness, and it is usually generalized. Lesions are erythematous maculopapules with areas of confluence, but they may be urticarial, vesicular, or sometimes petechial ( Figs. 14.24 to 14.32 ). The palms and soles may be involved. The eruptions are more common in children than in adults. In most cases, the rash fades without pigmentation or scaling.

Viral exanthem. Symmetric erythematous maculopapular eruption.

Viral exanthems can present with a variety of patterns on the palms. Papules, vesicles, or diffuse erythema are seen.

Viral exanthem with a maculopapular and vesicular pattern on the palm.

Viral exanthems may have several patterns. A diffuse maculopapular, blanching rash is a common pattern. Vesicular, urticarial, and petechial lesions may predominate.

Viral exanthem with a papular urticarial pattern on the face.

The area behind the ears is a common place to find viral exanthems.

Gianotti–Crosti syndrome. Self-limited, benign exanthem of childhood; 1- to 10-mm, pruritic papules or papulovesicles, commonly limited to the extremities and face.

Gianotti–Crosti syndrome. With the exception of the pruritic rash, patients are typically asymptomatic and healthy.

Gianotti–Crosti syndrome. Epstein–Barr virus infection is the cause in many cases.

Treatment.

Treatment consists of relieving symptoms.