Painful ulcers on the lips and tongue - Clinical Advisor

Painful ulcers on the lips and tongue

Slideshow

  • Multiple erosions and shallow ulcerations fo the cutaneous and mucosal lips, gingiva and hard palate in an elderly woman. The erosions extended superiorly to the perinasal area and many were covered with hemorrhagic crust.

    Herpes stomatitis

    Multiple erosions and shallow ulcerations fo the cutaneous and mucosal lips, gingiva and hard palate in an elderly woman. The erosions extended superiorly to the perinasal area and many were covered with hemorrhagic crust.

Clinical description

An elderly white woman was admitted to the hospital for management of an acute exacerbation of chronic obstructive pulmonary disease. Her treatment includes oxygen, inhaled bronchodilators, antibiotics, and oral corticosteroids.

The patient’s respiratory status was improved three days after admission, but she noted new painful ulceration of the lips and tongue. She also reported pain on swallowing and had a low-grade fever.

Examination revealed multiple erosions and shallow ulcerations of the cutaneous and mucosal lips, gingiva, and hard palate. The erosions extended superiorly to the perinasal area, and many were covered with hemorrhagic crust.



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On further questioning, the patient reported a history of occasional "cold sores" on the lips. A Tzanck smear of the base of an erosion on the tongue revealed abundant acute inflammatory cells as well as multinucleated giant epithelial cells. A...

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On further questioning, the patient reported a history of occasional “cold sores” on the lips. A Tzanck smear of the base of an erosion on the tongue revealed abundant acute inflammatory cells as well as multinucleated giant epithelial cells. A viral culture confirmed the diagnosis of recurrent herpes simplex virus (HSV)-1 stomatitis.

HSV is a common cause of orolabial infection. The causative agent is a double-stranded DNA virus that primarily infects its host through mucocutaneous exposure before establishing latency in nerve ganglia. Later reactivation of disease often ensues.

HSV is part of a larger family of viruses termed “human herpesviruses,” of which eight clinically relevant entities have been identified and numbered. There are two HSVs, designated HSV-1 and HSV-2. Other members of the human herpesvirus family include varicella zoster virus, Epstein-Barr virus, cytomegalovirus, and the causative agents of roseola infantum (also known as “sixth disease”) and Kaposi’s sarcoma.

HSV-1 primarily causes orolabial infection, while HSV-2 is typically a sexually transmitted disease causing genital infection. However, HSV-2 can also cause orolabial disease and is clinically indistinguishable from HSV-1. Both viruses are common, but HSV-1 is nearly ubiquitous, with 80% to 90% of adults demonstrating seropositivity for antibodies to HSV-1.1

Primary infection with HSV-1 occurs most often during infancy and early childhood (age 6 months to 5 years) or in early adulthood (age 20 to 25 years).2 The virus is spread through direct contact with contaminated saliva. The prevalence of HSV-2 is on the rise, and primary infection occurs most often in young adults and adolescents due to its sexual transmissibility.

The clinical features of both primary and recurrent HSV-1 infection are quite variable. The overwhelming majority of children are asymptomatic at the time of infection, and the primary stage may go unnoticed. Following a latency period of two to 20 days, symptomatic patients may develop a low-grade fever and painful vesicular eruption affecting the lips, buccal mucosa, gingival, and palate.

The primary lesions are small 2- to 3-mm vesicles that cluster and erode. Confluence of the erosions yields irregular ulcers with scalloped borders. A necrotic pseudomembrane and/or hemorrhage crust may develop secondarily. The eruption characteristically resolves spontaneously in approximately two to four weeks.

Because the virus resides dormant in sensory nerve ganglia, recurrence may ensue. Reported triggers of recurrence include: fever or concomitant illness, UV light, emotional stress, immunosuppression, and oral or facial surgery.1

Recurrent orolabial herpes is less dramatic and severe than a case of symptomatic primary infection. Recurrent disease may be restricted to the vermillion lips and typically runs a shorter course. The exception to this statement is in immunocompromised patients. In the case presented here, a more florid eruption of recurrent HSV-1 can be attributed to iatrogenic immunosuppression from corticosteroid therapy.

HSV infection may be complicated by dissemination in patients with pre-existing skin disease leading to a disrupted skin barrier. Disseminate HSV in this setting is referred to as “Kaposi’s varicelliform eruption” and may be seen in patients with atopic dermatitis (eczema herpeticum), Darier disease, and mycosis fungoides.

The differential diagnosis for herpes stomatitis includes other infections, autoimmune blistering disease, and drug hypersensitivity reactions. Oral ulceration may be seen in herpangina and hand-foot-mouth disease, but these ulcers favor the posterior pharynx and are not characteristically hemorrhagic or crusted.

Oral candidiasis can be erosive but often has an associated white plaque (thrush). Autoimmune blistering diseases, including pemphigus vulgaris, mucous membrane pemphigoid, and paraneoplastic pemphigus, should be considered in the differential diagnosis, especially when herpes-specific treatment fails.

Additional diagnostic entities to consider include mucositis and Stevens-Johnson syndrome (SJS). SJS may in fact be triggered by HSV infection, especially in young adults.

The diagnosis of herpes stomatitis may be made through different laboratory tests. A Tzanck smear is performed by scraping the base of an erosion or vesicle and transferring the fluid to a microscope slide. A stain is applied (Wright’s or Giemsa), and the specimen is then analyzed for viral cytopathic effect evidenced by multinucleation of giant epithelial cells.

Viral cytopathic effect may also be evident on tissue biopsy submitted for histopathology. More modern techniques include direct fluorescent antibody assay, and viral culture remains the gold standard of diagnosis.

Once diagnosis of herpes stomatitis is established, treat with antiviral agents. Options include acyclovir, valacyclovir, and famciclovir. For primary infection, oral acyclovir for seven to 10 days is usually sufficient. IV acyclovir may be necessary in severe cases of primary infection or in immunocompromised patients. Recurrent disease requires shorter treatment regimens. For uncomplicated cases, valacyclovir may also be used and has the advantage of a more convenient dosing schedule due to increased bioavailability.

The patient presented here was initially treated with IV acyclovir, 5 mg/kg t.i.d. Her mucocutaneous lesions rapidly improved, and she was transitioned to oral acyclovir to complete a seven-day course.

Dr. Travis Vandergriff, MD, is a dermatology resident at the University of Texas Southwestern Medical Center in Dallas. The author has no relationships to disclose relating to the content of this article.


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References

1. Arduino PG, Porter SR. Herpes Simplex Virus Type 1 infection: overview on relevant clinico-pathological features. J Oral Pathol Med. 2008;37:107-121.

2. Nasser M, Fedorowicz Z, Khoshnevisan MH, Shahiri Tabarestani M. Acyclovir for treating primary herpetic gingivostomatitis. Cochrane Database Syst Rev. 2008;4:CD006700.

All electronic documents accessed January 15, 2011.

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