Infective stomatitis

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Herpetic stomatitis

Aetiology A primary infection of a non-immune individual by HSV (usually) type 1. There is a steadily declining incidence in developed countries but increased prevalence in immunodeficiency, e.g. AIDS.

Pathology Viral infection of epithelial cells produces intraepithelial vesicles (Fig. 134) with virus-damaged cells in the floor (Fig. 135) leading to epithelial destruction (Fig. 136), ulcers and inflammation.

Smears from early lesions show ballooning degeneration of epithelial cell nuclei (viral proliferation pushing chromatin to form peripheral rim) and epithelial giant cells (Fig. 137).

There is a systemic febrile illness, lymphadenopathy, and a rising litre of antibodies.

Herpes labialis

Virus may persist in the trigeminal ganglion. Periodic reactivation leads to vesicles and crusting ulcers on borders of lips in about 30% of patients after primary infection. Microscopic features arc the same as for primary infection.

Herpes zoster of the trigeminal area

Aetiology Reactivation of varicella-zoster infection, usually in the elderly long after the initial infection (chickenpox). The condition is especially common and severe in immunodeficiencies; life-threatening in AIDS. Acyclovir is an effective anti-herpetic drug, but must be given in heavy dosage, especially to immunodeficient patients, and preferably intravenously.

Trigeminal zoster affects the sensory area of skin and mucosa of the affected division, usually unilaterally and typically with aching pain.

Microscopy Vesiculation and ulceration, the same as for herpes simplex.

Ballooning Degeneration Herpes

■ ' -ksmtmm fig. 134 Herpetic stomatitis: intact vesicle.

■ ' -ksmtmm fig. 134 Herpetic stomatitis: intact vesicle.

fig. 135 Herpetic stomatitis: virus-damaged cells in floor of vesicle.


fig. 136 Herpetic stomatitis: necrosis of epithelium.

fig. 137 Ballooning degeneration of epithelial cells in smear.

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