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A Puzzling Facial Rash on a 17-Year-Old Boy

http://cme.medscape.com/viewarticle/575109_2

Background

A 17-year-old male high school student presents to the pediatric infectious disease clinic complaining of a 10-day history of a facial rash that "won't get better." The patient had previously visited his primary care provider (PCP), who started the patient on amoxicillin-clavulanic acid 8 days ago. The rash did not improve on the antibiotic, and as a result, it was discontinued and the patient switched to trimethoprim-sulfamethoxazole. No improvement was noted with the second round of antibiotic therapy; the rash continued to spread, and the lesions increased in number. The patient was subsequently advised to follow up with the infectious disease clinic.

At the infectious disease clinic, the patient states that the rash started with several pimples over the forehead and cheek and then continued to spread and involve most of the right side of his face. The lesions are not itchy, but they are painful. The patient has no known drug allergies. His immunizations are up to date. He is very active on the wrestling team and was happily preparing for an upcoming competition. The patient denies having any weight loss, headaches, dizziness, photophobia, fever, or chills. The family history is non-contributory.

On physical examination, the patient is alert and orientated. His oral temperature is 97.0°F (36.1°C). The patient has normal heart sounds, his pulse has a regular rhythm of 97 bpm, and his blood pressure is 125/75 mm Hg. His lungs are clear, and his respiratory rate is 12 breaths/min. The examination of the head, eyes, ears, and nose is remarkable for multiple vesicular lesions measuring about 0.5 cm in diameter (see Figures 1 and 2). There is bilateral submandibular lymph gland enlargement measuring 1.5 cm by 1 cm. The neck is supple. His abdomen is soft and nontender to deep palpation in the epigastric region, and no organomegaly is noted. A complete blood count (CBC) taken at the PCP's office showed a white blood cell (WBC) count of 7.4 × 103/µL (7.4 × 109/L), with a normal differential; a hemoglobin of 13.6 g/dl (136 g/L); a hematocrit of 38.3% (0.3830); and a platelet count of 298 × 103/µL (298 × 109/L).


Hint: The patient was disqualified from wrestling because of his lesions.
 Tinea faciale
 Impetigo
 Bacterial cellulitis
 Herpes gladiatorum


Discussion:

Herpes gladiatorum (HG) is an infection caused by the herpes simplex virus (HSV) type 1. HG most commonly occurs among wrestlers and other athletes who participate in close skin contact sports such as wrestling (herpes gladiatorum) and rugby (herpes rugbiaforum). HG is also known as "mat herpes" among wrestlers. HG is spread by direct skin-to-skin contact. The lesions appear within 7 to 14 days after exposure; however, in some cases the lesions take longer to appear. Our patient presented with a primary herpes gladiatorum (PHG) infection, which is usually more severe than the recurrent infections. His lesions presented with disseminated vesicles, punched-out erosions, and central crusting on the forehead and right cheek. The patient was at an increased risk of contracting PHG because of his participation in wrestling. Herpes simplex virus DNA was detected with a polymerase chain reaction (PCR) examination.[3,6]

Outbreaks of HG have occurred countless times during the last decade; several outbreaks of HG have occurred among wrestlers across the United States. It is critical that health care providers, athletic trainers, coaches, and athletes recognize the threat of HG skin infection to minimize the risk of outbreaks. Vigilant surveillance and appropriate antiviral treatment will curtail the transmission of HG among wrestlers.[7] Lack of proper understanding of PHG disease could lead to misdiagnosis and frequent outbreaks.[4]

HSV is a double-stranded DNA virus. About 80% of adults have antibodies to HSV-1, and about 20% of the population has antibodies to HSV-2. HSV-1 is commonly known to cause herpes labialis and keratitis. Most childhood HSV infections are caused by HSV-1. HSV-2 is commonly known to cause genital herpes infections, which is one of the most common sexually transmitted diseases in the United States. HSV-2 is transmitted primarily by direct contact with lesions, and it is most often transmitted venereally. Generalized or localized cutaneous and mucosal lesions characterize initial infection by HSV. Recurrent infections are milder because fewer viruses are shed and a stronger immune response is elicited. HSV remains dormant in the nerve ganglia; febrile illness, stress, immunosuppressive drugs, and ultraviolet light can precipitate recurrent eruptions. In rare cases, the initial replication of HSV can lead to meningitis or encephalitis. HSV persists for life in a latent form. The virus is sometimes confused with herpes zoster because the site of latency for HSV is the trigeminal ganglion. HSV may also manifest as a severe and/or life-threatening infection in immunocompromised individuals and in newborn babies. Specifically, disseminated infections can result in esophagitis, pneumonitis, encephalitis, hepatitis, and adrenal necrosis.[1,3]

Currently, no epidemiologic studies accurately identify the true incidence of HG; however, the National Collegiate Athletic Association (NCAA) estimated an incidence of HG as high as 40% among wrestlers.[2] The most common locations of HG, in descending order, are the head, face, neck, chest, and shoulders. Typically, lesions will be observed on the head, face, neck, cheeks, forehead, shoulders, and arms. According to most studies, about two thirds of wrestlers will have the herpetic lesions on the right side of the body. Hence, HG is transmitted during close skin-to-skin physical contact, known in wrestlers' terminology as the "lock-up position."[1,6]

PHG generally presents with an erythematous rash, sore throat, fever, cervical lymphadenopathy, and vesicles. Occasionally, the HG lesion will lack the grouped vesicles on an erythematous base, and it is sometimes mistaken for impetigo, acne, tinea corporis, atopic dermatitis, varicella, or scabies. A significant complication of PHG in wrestlers is dendritic keratitis with subsequent corneal scarring. Other ocular complications of PHG include conjunctivitis, scleritis, and uveitis. Fluid from the base of unroofed vesicles can be sent for testing by PCR, the test of choice for diagnosing PHG. A Tzanck smear of scrapings from the base of vesicles will demonstrate multinucleated giant cells, a finding that is highly indicative for HSV infection.

The NCAA has developed recommendations on "time until return to competition" for primary herpes gladiatorum and for recurrent infection. For a primary outbreak of herpes, the wrestler must be examined by a clinician or an experienced certified athletic trainer; the following recommendations must be met before a wrestler returns to competition[7]:
The athlete must have no signs of systemic symptoms of viral infection.

The athlete must be free of any new lesions for 3 days or more prior to start of competition.

The skin lesions must be dried and surmounted by a firm adherent crust.

The athlete must have been on appropriate antiviral therapy for at least 120 hours before the beginning of a competition.

For recurrent HG, the NCAA has also established several recommendations. First, vesicles must be completely dry and crusted. Second, the wrestler must have been on the appropriate dosage of antiviral therapy for 120 hours or more at the time of tournament. For questionable cases, a Tzanck preparation should be performed, and the wrestler's status should be deferred until Tzanck prep or HSV assay results are available.[7]

Antiviral drugs with activity against viral DNA synthesis have been effective against PHG infections. Acyclovir, famciclovir, and valacyclovir inhibit virus replication and suppress clinical manifestations, but they are not a cure for PHG, since HSV remains latent in sensory ganglia. Oral acyclovir has been shown to be effective in suppressing PHG in wrestlers; it is the drug of choice for treating PHG. Acyclovir reduces the duration of symptomatic lesions and is indicated for patients presenting within 2-3 days of the appearance of a herpetic rash. Most patients on acyclovir will experience less pain and quicker resolution of their vesicular lesions. Several effective treatments for adult patients include oral acyclovir 200 mg 5 times daily or 400 mg 3 times daily for 7-10 days or until clinical resolution occurs. The recommended dose of acyclovir for PHG in the pediatric age group is 20-30 mg/kg/d, in 5 divided doses, for 7-10 days. As with all infections, prevention is better than treatment.[2]

In addition to the above treatment, wrestlers must practice effective hygiene immediately after wrestling. It is critical to frequently clean competition gear and change towels. Regular hand-washing and thorough cleaning of the mats are critical. Wrestling mats should be cleaned between matches with household bleach (one-quarter cup of bleach in 1 gallon of water). Early identification and treatment can allow the wrestler to return to participation earlier and prevent teammates from contracting the disease. Despite these precautions, PHG will spread during wrestling and other close-contact sports resulting from contact with asymptomatic infected athletes.[1,6]

The patient in this case was started on acyclovir 400 mg 3 times a day for 1 week at the first visit to the pediatric infectious disease clinic. It was strongly suspected that his lesions were caused by PHG, since there had been no improvement with the 2 courses of antibiotic treatment that had been initially tried by his primary care provider. After 1 week of acyclovir, most of his facial lesions were dry and had an adherent crust; however, there were still 2 moist lesions on his right shoulder, which resolved completely by the second week of treatment. The patient and his parents were advised repeatedly to call and report any eye symptoms, seizure, alteration of mental status, personality changes, photophobia, or headaches. It was noted on subsequent follow-up that the patient's 13-year-old brother had developed similar lesions; it was later learned that he had borrowed his older brother's headgear, which was the most likely the cause of his lesions. The rash on the brother also resolved after starting acyclovir.