What Is This Expanding Leg Lesion?
THE CASE: A 16-year-old girl presents to an acute care pediatric clinic with a worsening lesion on her shin 3 days after she was discharged from the hospital. She had presented to the emergency department (ED) 5 days earlier because of mild respira-tory distress and a 4-day history of odynophagia and enlarged cervical lymph nodes. She was noted to have a coarse voice, bilateral 41 tonsillar enlargement and anterior cervical lymphadenopathy, an enlarged inguinal lymph node of the right leg, and a nontender abdomen with no organomegaly. She also had a single erythematous papule on her right shin.
Infectious mononucleosis was diagnosed on the basis of the clinical presentation and positive results of a monospot test. The patient was admitted to the hospital for treatment with oral corti-costeroids for respiratory distress. She was discharged within 2 days.
On presentation to the acute care pediatric clinic, the single papule on her leg had enlarged and become vesicular, as shown. The lesion is nontender and nonpruritic. The patient’s past dermatologic history is significant for linear verrucous epidermal nevus and irritant contact dermatitis. She is in high school and plays no contact sports. She has no psychosocial risk factors, recent travel, past history of herpes infection, or unusual exposures.
What is the likely cause of this leg lesion?
A. DNA poxvirus.
B. Epstein-Barr virus.
C. Herpes simplex virus.
D. Staphylococcus aureus.
(Answer on next page)
The correct answer is C, Herpes simplex virus.
Discussion: A Gram stain of fluid from a vesicle was negative. However, a Tzanck smear performed by a dermatologist revealed multinucleated giant cells, and herpes simplex virus (HSV) was detected by polymerase chain reaction (PCR). Culture was negative for bacteria. Although oral antivirals can be prescribed
to treat HSV, the lesion began to crust and heal within a few days without treatment. The patient was counseled that this herpes skin infection is spread by direct skin-to-skin contact and prevention was discussed.
This case demonstrates an unusual location for cutaneous HSV infection in an adolescent with no risk factors, such as history of herpes infection and participation in contact sports. Herpes skin infection acquired during wrestling—the sport most often associated with this condition—is known as herpes gladiatorum.
The HSV lesion in this patient may have represented primary infection or reactivation of dormant infection. Reactivated HSV infection may present as a vesicular skin lesion or febrile illness. Multiple stressors, including hyperthermia, hypothermia, fatigue, and immunosuppression, may cause reactivation.1 Reactivation of HSV caused by alteration of immunity, which can occur with infectious mononucleosis, is a distinct possibility in this case. Psychological and social stress may also lead to alterations in the immune system.
A Tzanck smear and HSV PCR can confirm a clinical diagnosis, suspected on the basis of the classic vesicular appearance of the lesion. Although HSV infection is associated with significant morbidity and mortality in newborns and immunocompromised persons, the infection in an otherwise healthy individual is typically benign and self-limited. However, it can cause an athlete to miss playing time. Clinicians should consider HSV infection in the differential diagnosis for any acute vesicular lesion. Timely diagnosis may prevent transmission and allow for early initiation of antiviral therapy, if indicated.
Dermatologic conditions associated with Epstein-Barr virus, the major cause of infectious mononucleosis, include a transient erythematous, maculopapular rash on the trunk and extremities that occurs with antibiotic administration; erythema multiforme, a granuloma annulare–like eruption predominantly involving the face and arms; and a variety of cutaneous and mucosal manifestations, including genital ulcers.2-5
Molluscum contagiosum, caused by DNA poxvirus, is characterized by flesh-colored papules with depressed centers that can occur in crops.
Staphylococcus aureus can cause bullous impetigo, which appears as a cluster of vesicles and blisters that can rupture and result in denuded areas.