Genital ulcer and viral warts
Department of Dermatology, Venereology and Leprology, PG I MER Chandigarh - 160 012
|How to cite this article:
Kumar B, Muralidhar S. Genital ulcer and viral warts. Indian J Dermatol Venereol Leprol 1997;63:213-214
To the Editor
Genital ulcers are known to increase the acquisition of HIV infection and chancroid especially is well known factor. However, the relation between genital ulcer and another virus viz. HPV responsible for genital warts is not known. One patient who developed genital ulcer and a genital wart after an incubation period of less than a week, sheds some light on the relationship between these two common STDs and also the management problems in this part of the world.
This patient is a 22-year-old bachelor, who after his only sexual experience with a commercial sex worker developed painful genital ulcers after an incubation period of 5 days. On examination he had two painful, nonindurated ulcers covered with purulent exudate and oedematous prepuce. No regional adenopathy and other concomitant STDs were observed.
A diagnosis of chancroid was made and all side lab investigations in relation to ulcer including dark-field microscopy, tissue smear, Tzanck smear, Gram stain and surface swab for culture of H ducreyi were done. All investigations were negative. His blood VDRL and HIV serology were non reactive. Patient was treated with single oral dose of 500mg of ciprofloxacin.
On re-examination of the patient, 5 days after treatment, a filiform wart was noted emerging from ulcer (Fig-1). The ulcer healed in 10days and the warts were cauterized with trichloroacetic acid. There is every possibility that the wart was present even at the first visit but a small lesion could not be appreciated in the active granulation tissue and it became apparent only after the ulcer had partially healed.
Genital warts manifest after an incubation period of 3 weeks to 8 months (mean 2.8 weeks). The patient developed a wart within a short span of 10days which could be due to concomitant infection with H ducreyi. Human papilloma virus resides in keratinocytes and their proliferation during the inflammatory phase of chancroidal ulcer might have led to the early manifestation of HPV. Various cytokines including TNF are released in inflammatory conditions. TNF is known to upregulate HIV infection through cellular inductive signals. Similar mechanisms may also operate in HPV infection. Epidermal growth factors by stimulating keratinocytes are involved in wound healing and thus epidermal growth factor through keratinocyte proliferation might have indirectly led to the proliferation of HPV.
Apart from this interaction between two common STDs, the presence of wart in an ulcerated area led to management problem. Podophyllin an effective and commonly used drug cannot be applied over a raw area. Hence, trichloroacetic acid was applied to the warts though cryotherapy might have been a better choice if available.
This case highlights the significance of concomitant STDs and the problem in their management.
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