Oral Herpes Infections
On this page
Direct answer
Fever, drooling and crops of fragile vesicles on an angry, swollen gingiva in a preschool child point to primary herpetic gingivostomatitis, the commonest clinical manifestation of initial HSV-1 infection and a self-limiting illness of seven to fourteen days. After primary infection the virus retreats to the trigeminal ganglion, from where fever, sunlight, stress or menstruation can reactivate it as herpes labialis — the recurrent cold sore preceded by a tingling prodrome. The differential family includes varicella-zoster with its strictly unilateral, dermatomal vesicles, Coxsackie-virus herpangina confined to the soft palate and tonsillar pillars, and hand-foot-mouth disease with its matching peripheral rash; a Tzanck smear showing multinucleated giant cells supports a herpesvirus diagnosis.
What you must remember
- Primary herpetic gingivostomatitis typically affects children between six months and five years as maternal antibody wanes; vesicles rupture into small, coalescing ulcers on keratinized and non-keratinized mucosa alike, with fever and cervical lymphadenopathy.
- Management of primary herpes is supportive — hydration, soft diet, analgesia and chlorhexidine rinses — with systemic aciclovir reserved for the immunocompromised or the child deteriorating early in illness.
- Recurrent herpes labialis is heralded by a tingling or burning prodrome; topical aciclovir or penciclovir works only if started in that window, and intraoral recurrence sits on hard palate and attached gingiva, mimicking other ulcers.
- Herpes zoster: reactivation of varicella-zoster virus in a single trigeminal division; vesicles stop strictly at the midline, pain may precede the rash, post-herpetic neuralgia is the feared sequel, and geniculate ganglion involvement produces Ramsay Hunt syndrome with facial palsy and ear vesicles.
- Herpangina (Coxsackie A types) produces summer-season vesicles and ulcers of the soft palate and tonsillar pillars with high fever but no gingival involvement; hand-foot-mouth disease (classically Coxsackie A16) adds maculovesicular lesions on palms and soles.
- A Tzanck smear of an unroofed vesicle showing multinucleated epithelial giant cells suggests herpes simplex or zoster; definitive confirmation is by antigen detection or PCR.
- Gloves matter: dental professionals treating active HSV lesions have contracted herpetic whitlow of the finger through gloveless or careless contact.
Managing the child with primary herpes
A three-year-old arrives febrile, refusing food, with vesicles and yellow ulcers studding the gingiva, palate and tongue, and tender submandibular nodes. The first task is recognition — primary herpes, not aphthous stomatitis (no prodrome, no fever, no vesicular stage, no keratinized-mucosa preference) and not ANUG (which excavates interdental papillae in older patients). Second, supportive care with measurable goals: wet diapers and oral fluids counted at home, paracetamol by weight, and chlorhexidine gel to limit secondary infection. Third, thresholds for escalation — dehydration, inability to swallow, immunocompromise, or eczema (risk of eczema herpeticum) send the child for hospital admission and intravenous aciclovir. Fourth, hygiene teaching, since saliva spreads virus to siblings and caregivers, and the clinician protects her own fingers with gloves. The episode resolves within two weeks; the family should then know the virus remains for life and may return as cold sores.
Recurrent herpes or aphthous ulcer?
Both present as painful oral ulcers, and the mix-up misdirects both diagnosis and treatment. The discriminator is anatomy: recurrent intraoral herpes breaks out on keratinized, firm mucosa — hard palate, attached gingiva — as a tight cluster of tiny, coalescing ulcers, often after dental treatment or trauma triggers it; aphthae favour the movable, non-keratinized mucosa of lips, cheeks, floor of mouth and soft palate as solitary or few larger ulcers. The student who remembers "hard mucosa herpes, soft mucosa aphthous" answers this viva in one line, and the clinician who applies it avoids prescribing antivirals for aphthae or steroids alone for herpes.
Frequently asked questions
What is the classic age for primary herpetic gingivostomatitis?
Between six months and five years, as maternally derived antibodies fade; many infections are subclinical, which is why adults can develop primary disease too.
Where does HSV-1 establish latency?
In the trigeminal ganglion, from where it reactivates along sensory nerves to produce herpes labialis or intraoral recurrent lesions.
When should aciclovir be given in primary herpes?
Early in the illness for immunocompromised or severely affected children, and within the prodrome for recurrent labialis; late topical treatment of an established sore adds little.
How does zoster differ from intraoral herpes simplex?
Zoster is unilateral and respects the midline within one dermatome, causes deep pain that may precede vesicles, and can leave post-herpetic neuralgia; herpes simplex recurs locally without dermatome boundaries.
Which virus causes herpangina, and where are the lesions?
Coxsackie group A viruses, producing posterior lesions on the soft palate, tonsillar pillars and pharynx in summer outbreaks among children, without gingival involvement.
What is herpetic whitlow?
Painful HSV infection of the finger, historically an occupational hazard for dental surgeons contacting saliva without gloves — the reason gloves are mandatory for every patient.