A 12-month-old previously healthy boy is seen in the office with a 3-day history of fever and ulcerative lesions on his lips and mouth. Over the past day the lesions had spread to his face and around his eye (Figure 39-1). His mother has noted that the lesions have evolved from flat to raised lesions to fluid-filled ulcers. The boy has been irritable, and over the past day, has refused to eat and drink. He appears dehydrated and is admitted to the hospital for intravenous fluid hydration.

Primary herpes simplex virus (HSV) infection occurs commonly in infants and children. While most infections are asymptomatic, the most common clinical manifestation of primary HSV infection is gingivostomatitis. This infection in otherwise healthy infants and children is self-limited, but can occasionally lead to dehydration and hospitalization. Immunocompromised individuals who are infected with HSV may have more severe and systemic manifestations.

Oro-labial HSV infection; cold sores; fever blisters; herpetic stomatitis.

• Most perioral HSV infections are asymptomatic; thus, manifestations of HSV infections are apparent in a small proportion of patients who become infected.¹

• Primary infection with HSV-1 usually occurs in infants and children.²

• Acquisition occurs after mucocutaneous contact between a susceptible host and a contact who is shedding the virus.

• Transmission occurs commonly from an asymptomatic individual who is shedding the virus after primary infection or after reactivation of the virus.

• Incubation period is 3 to 4 days.

• Most infections are caused by HSV-1.

• Primary infection occurs when the virus penetrates through abraded skin or mucosal surfaces.

• HSV enters cutaneous neurons and then migrates to the sensory ganglia, where the virus replicates and then returns to the inoculation site via peripheral sensory ganglia.³

• Skin and mucous membrane changes are more severe following primary infection than following reactivation of the virus.

• Establishment of lifelong latency is a hallmark feature of all herpes viruses; latency is established in the trigeminal ganglia.

• Periodic reactivation of the virus occurs, resulting in spread of the virus down the neuroaxis, causing shedding of the virus and possible recurrent skin lesions.

• Possible triggers of reactivation of HSV include stress, exposure to ultraviolet light, intercurrent infections, manipulation of nerve roots, dental manipulation, hormonal changes, and immunosuppression.

Clinical Features

Primary infections

• Fever, irritability, and tender submandibular lymphadenopathy are common in symptomatic patients.

• Vesiculo-ulcerative lesions can occur on the palate, gingiva, tongue, lip, and face (Figures 39-2 and 39-3).⁴

• Lesions are associated with pain and intraoral edema (Figure 39-4).

• Involvement of the peri-orbital area can occur via autoinoculation or as a manifestation of the primary infection (Figure 39-5).

• Lesions evolve from vesicles to shallow ulcers on an erythematous base.

• Lesions may last 2 to 3 weeks.

• Inability to take oral liquids and solids is common.

• Most common cause of hospitalization is dehydration.

• Immunocompromised patients may have more severe involvement of the mouth and face, and may evolve into disseminated disease (Figure 39-6).