An 8-year-old boy suddenly develops a facial rash. During the initial teledermatology consultation, it was learned that the eruption first appeared 3 days earlier; the rash is not pruritic. According to the patient’s parent, the boy has no fever but experienced a runny nose prior to the onset of the rash. He is otherwise in good health. The parents forwarded a photograph of the patient (Figure), which illustrates a striking erythematous eruption on his face.
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Erythema infectiosum was originally believed to be a milder form of rubella or measles. It was first designated as fifth disease in the early 1900s when infectious exanthems were numbered first through sixth.1 It is caused by a viral infection with parvovirus B 19, a nonenveloped, single-stranded DNA virus belonging to the Parvoviridae family.2 The term “slapped face syndrome” describes the characteristic facial rash.3
The parvovirus only infects humans and has a life cycle similar to that of other nonenveloped DNA viruses. This includes binding to host cell receptors and entering cells of the respiratory tract resulting in translocation of its genome to the host nucleus followed by assembly of viral capsids.4 Viremia occurs 8 to 10 days after inoculation.
This common childhood infection classically presents as a mild febrile illness with rash that is self-limited in immunocompetent hosts.5 The prodrome is characterized by low-grade fever, malaise, sore throat, headache, and nausea followed several days later by an erythematous “slapped cheek” facial rash. Once the facial rash fades, children may develop pink patches and macules in a lacy, reticular pattern most often on the extremities. The later course of infection can also present with arthralgias affecting the hands, feet, wrist, knees, and feet.
Erythema infectiosum most commonly occurs in children aged 5 to 15 years; typically in the spring months. While the disease is usually mild, in certain high-risk groups it can have serious consequences. In pregnant patients, complications include miscarriage, intrauterine death, and hydrops fetalis.6 Individuals with sickle-cell anemia can develop aplastic crisis and severe anemias.7
Differential diagnosis includes other viral exanthems such as measles, rubella, roseola, and scarlet fever. Laboratory testing is usually unnecessary because of the self-limiting nature of the disease and mild symptoms. Assay of the blood work for the specific immunoglobulin M (IgM) parvovirus B 19 antibody can confirm an acute infection as can polymerase chain reaction testing.8
Alexandra Stroia, BS, is a medical student at the Lake Erie College of Osteopathic Medicine in Erie, Pennsylvania; Stephen Schleicher, MD, is director of the DermDox Dermatology Centers, associate professor of medicine at Geisinger Commonwealth Medical College, and clinical instructor of dermatology at Arcadia University and Kings College.
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