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Case Reports
Patient 1
A 29-year-old man who was seropositive for the human immunodeficiency virus (HIV) was admitted with cryptococcal meningitis, and a morbilliform eruption presumed to be due to one of his medications subsequently developed. He also had coalescing erosions on his lower lip and numerous tender linear fissures in a cross-hatched pattern on the dorsum of his tongue. Viral cultures from both the lip and the tongue grew HSV type 11. Oral acyclovir (200 mg five times daily) was started. The patient's tongue pain resolved within 2 days, and all his lingual lesions had healed after 12 days of therapy; a post-treatment viral culture of the tongue was negative.
Patient 2
A 37-year-old man with systemic lupus erythematosus who was seropositive for HIV was admitted with Pneumocystis carinii pneumonia. The patient had World Health Organization class IV lupus nephritis requiring treatment with prednisone at a dose of 150 mg every other day. In the hospital, the dose was increased to 40 mg twice a day and trimethoprim-sulfamethoxazole was started. There was cutaneous Kaposi's sarcoma on the penis. The patient also had a painful transverse fissure, 2 cm in length, on the dorsum of his tongue. A viral culture from the fissure grew HSV type 1, and treatment with oral acyclovir was begun. The fissure healed by the 12th day of hospitalization.
Patient 3
An alcoholic 41-year-old man who was seropositive for HIV and had a history of pancreatitis was admitted to the hospital for diabetic ketoacidosis. He had hypertrophic scars on the right precordial area and a bright red, smooth anterior tongue with two painful longitudinal fissures, 5 mm in length, at the tip; a 4-cm area on the dorsum with exquisitely tender cross-hatched fissures; and angular cheilitis of the right oral commissure. A viral culture taken from the dorsal fissures grew HSV type 1. The patient's lingual symptoms and fissures resolved after treatment with oral acyclovir.
Patient 4
A 27-year-old woman who was seropositive for HIV had a severe allergic reaction to trimethoprim-sulfamethoxazole and was hospitalized. She had no mucosal lesions. On the third day of hospitalization she had an acute attack of respiratory decompensation that was initially thought to be due to P. carinii pneumonia. Bronchoscopy was performed, and empirical treatment with intravenous pentamidine and corticosteroids was begun. Three days later, a painful linear fissure that was 5 cm long and had a branched pattern developed on the dorsum of the tongue (Figure 1). Treatment with oral acyclovir was begun after the viral cultures obtained from the fissure grew HSV type 1. The bronchial-lavage fluid and the lung biopsy were negative for both P. carinii and HSV; the pneumonitis was presumed to be due to the adverse reaction to trimethoprim-sulfamethoxazole. Pentamidine was discontinued, and the systemic corticosteroids were tapered. Ten days after acyclovir therapy was begun, the patient was discharged. At that time, her tongue was free of pain and the fissure had almost healed.
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A 49-year-old woman who was seropositive for HIV and had progressive, multifocal leukoencephalopathy was admitted with cortical blindness. Treatment with dexamethasone in a dose of 4 mg every six hours was begun. A leg lesion was thought to be Kaposi's sarcoma. Physical examination of the right thigh revealed a dermatofibroma. Four tender linear erosions, 4 to 8 mm in length, were also noted on the dorsum of the tongue. A viral culture taken from the tongue lesions grew HSV type 1. The tongue symptoms and fissures healed completely after three days of oral acyclovir.
Discussion
HSV infections in the immunocompromised host are atypical in location, appearance, and behavior. The classic evolution from erythematous papules to vesicles to ulcer is rare. This process appears to be accelerated in the compromised host, because the lesions often first appear as ulcerations.
Oral HSV lesions in the immunocompromised host involve all intraoral and oropharyngeal sites, not just the attached tissue of the keratinized gingiva and hard palate2,3. The tongue, buccal mucosa, floor of the mouth, and soft palate may be affected. When the tongue is involved, the lateral surface is usually affected4. Therefore, HSV on the dorsum of the tongue is atypical and unexpected.
Oral HSV infections may have myriad forms, including crater-like ulcers with white, raised borders containing small vesicles; diffuse erythema mimicking bacterial mucositis; coalesced yellow papules resembling candidiasis; an isolated tongue ulceration that appears to be due to trauma; and an exophytic, dark red, superficially ulcerated nodule on the dorsum of the tongue3,4,5,6,7. The differential diagnosis includes ulcers due to trauma (from dental work or other manipulations) or neutropenia, mucositis caused by chemotherapy or radiotherapy, fungal or bacterial infections, and oral lesions such as aphthous stomatitis or erythema multiforme seen in otherwise healthy persons. Ulcers caused by HSV infection may become secondarily infected with bacteria or fungi, making it difficult to recognize the true nature of the primary problem7.
Tongue lesions caused by HSV infection are characteristically painful and may impair oral intake. The lesions break the mucosal integrity and provide a portal of invasion for other infectious agents, including the normal oral flora. Herpetic lesions in immunocompromised hosts are often more numerous and invasive, cause greater pain, produce deeper ulcerations, are slower to heal, and shed virus longer than do such lesions in immunocompetent persons. These observations underscore the importance of the prompt recognition and treatment of atypical HSV infections.
Source Information
From the Dermatology Consultation Service, Columbia-Presbyterian Medical Center, New York (M.E.G., A.W.S.); the Departments of Dermatology and Pathology, University of Texas-Houston Medical School, Houston (P.R.C.); and the Department of Medical Specialties, Section of Dermatology, University of Texas M.D. Anderson Cancer Center, Houston (P.R.C.).
Address reprint requests to Dr. Grossman at the Department of Dermatology, College of Physicians and Surgeons of Columbia University, 630 W. 168th St., VC15-206, New York, NY 10032.
References
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Related Letters:
Herpetic Geometric Glossitis
Lam S., Lam B. L., Cohen P. R., Grossman M. E.
Extract |
Full Text
N Engl J Med 1994;
330:1393-1394, May 12, 1994.
Correspondence
This article has been cited by other articles:
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