BACKGROUND: Patients with HIV infection can have recurrent and persistent oral ulcers, not attributable to known infectious agents. OBJECTIVE: Our aim was to evaluate prospectively oral ulcers in patients with HIV infection to determine whether an etiologic agent could be identified. METHODS: Sixteen patients with HIV infection who had oral ulcers not attributable to known causes had culture of the base and a biopsy specimen taken from the ulcer. Cultures were obtained for herpes simplex and varicella-zoster viruses, mycobacteria, and fungi. By polymerase chain reaction (PCR) analysis with primer/probe sets for herpes simplex viruses 1 and 2, varicella-zoster virus, cytomegalovirus, human papillomavirus, and Mycobacterium tuberculosis, each biopsy specimen was analyzed for the presence of DNA from these organisms. Specimens were also evaluated histologically. RESULTS: Histoplasmosis was detected histologically in one biopsy specimen, candidiasis in a second, and herpetic changes in a third. Viral cultures were positive for herpes simplex virus 1 in four cases and herpes simplex virus 2 in one case. PCR analysis detected DNA for herpes simplex virus 1 in one case and herpes simplex virus 2 in another; DNA from other pathogens was not identified. In the remaining eight patients, hematoxylin-and-eosin staining revealed eosinophilic ulcers in five cases and nonspecific changes in three cases. CONCLUSION: The etiologic agent of recurrent or persistent oral ulcers in patients with AIDS and AIDS-related complex was not identified in 50% of patients. PCR analysis was not useful. Herpes simplex virus or other pathogens were not detected in ulcers containing numerous eosinophils.
BACKGROUND:Patients with HIV infection can have recurrent and persistent oral ulcers, not attributable to known infectious agents. OBJECTIVE: Our aim was to evaluate prospectively oral ulcers in patients with HIV infection to determine whether an etiologic agent could be identified. METHODS: Sixteen patients with HIV infection who had oral ulcers not attributable to known causes had culture of the base and a biopsy specimen taken from the ulcer. Cultures were obtained for herpes simplex and varicella-zoster viruses, mycobacteria, and fungi. By polymerase chain reaction (PCR) analysis with primer/probe sets for herpes simplex viruses 1 and 2, varicella-zoster virus, cytomegalovirus, human papillomavirus, and Mycobacterium tuberculosis, each biopsy specimen was analyzed for the presence of DNA from these organisms. Specimens were also evaluated histologically. RESULTS:Histoplasmosis was detected histologically in one biopsy specimen, candidiasis in a second, and herpetic changes in a third. Viral cultures were positive for herpes simplex virus 1 in four cases and herpes simplex virus 2 in one case. PCR analysis detected DNA for herpes simplex virus 1 in one case and herpes simplex virus 2 in another; DNA from other pathogens was not identified. In the remaining eight patients, hematoxylin-and-eosin staining revealed eosinophilic ulcers in five cases and nonspecific changes in three cases. CONCLUSION: The etiologic agent of recurrent or persistent oral ulcers in patients with AIDS and AIDS-related complex was not identified in 50% of patients. PCR analysis was not useful. Herpes simplex virus or other pathogens were not detected in ulcers containing numerous eosinophils.