A 29-year-old, HIV-infected African man (CD4 364 cells/μL and viral load < 150 copies/mL) presented to the King Edward VIII Hospital Infectious Diseases Clinic in Durban, South Africa, complaining of oozing pus from discrete areas over his glans penis with leaking of urine from those same areas on micturition. This illness evolved over the preceding 7 months. He was otherwise well and had initiated antiretroviral therapy 3 months earlier.
Initial genitourinary examination revealed a circumcised penis with two wart-like lesions in the dorsal sulcus oozing pus and five further small fistulas draining pus with frank pus oozing from the urethra (Figure 1). On voiding, 3/5 sinuses and one of the two cutaneous warts leaked urine, suggesting a connection between the urethra and the surface of the penis. He was given three courses of cefixime 400 mg oral stat, one course of doxycycline 100 mg 12 hourly for 7 days, and one course of metronidazole 2 g stat over the preceding 7 months with no impact on his symptoms. Cytological examination of the purulent material revealed squamous epithelial cells and suppurative inflammation. Organisms with features suggestive of Trichomonas vaginalis (TV) were observed. No acid-fast bacilli or malignant cells were noted. The patient was treated with KMnO4 soaks for the lesions.
On follow-up 2 months later, the patient reported no change in his condition. Physical examination was unchanged. Gram stain of purulent material revealed scanty leukocytes, gram-positive cocci, moderate gram-negative bacilli, and moderate gram-negative coccobacilli. Bacterial culture grew Enterococcus faecalis and Staphylococcus hyicus, susceptible to penicillin. Auramine O stain did not reveal any acid-fast bacilli, and mycobacterial culture was negative. Cytology again revealed the presence of TV accompanied by reactive cellular changes consistent with Trichomonas infection (Figure 2). There was no evidence of malignant cells or acid-fast bacilli. The persistent presence of Trichomonas led to treatment with metronidazole 400 mg 8 hourly for 14 days.
At the 2-week review, the patient reported resolution of the purulent discharge from the sinuses. Physical examination still revealed the warty lesion. A biopsy of the wart confirmed condyloma acuminatum with a background of chronic inflammation. At 3-week review, the patient reported marked healing of the sinuses/fistulae. On review 6 months later, all but one sinus had completely healed. A remaining discrete lesion oozed minimal fluid on pressure but not urine on micturition. Cytology of this fluid demonstrated cellular debris.
As far as can be determined, this is the first description of TV infection implicated as the probable cause of a destructive lesion leading to sinus drainage and fistula formation. Another similar presentation involving TV was reported. The authors in that case attributed the rectovaginal fistula to Behcet's disease and implicated TV infection in the pathogenesis of the Behcet's disease.1 In the current case, the only potential pathogen repeatedly noted was TV. Resolution of the lesion with metronidazole, which is unlikely to have addressed any other potential pathogen missed on microbiological testing, supports TV as the inciting pathogen.
In males, following an incubation period of about 10 days, trichomoniasis can result in asymptomatic carriage, a non-gonococcal-like urethritis and/or prostatitis.2 Several old reports have associated TV with urethral strictures in males.3–5 Furthermore, in vitro studies have demonstrated that TV produces virulence factors that can cause host cell damage contributing to tissue destruction and inflammation.6,7 These observations added weight to the possibility that TV is able to, directly or indirectly, cause tissue destruction and healing with fibrosis. In our patient, the condyloma acuminatum was considered an incidental sexually transmitted infection (STI) having no influence on this presentation of Trichomonas infection. This assumption was supported by the virtual complete resolution of the fistulous lesions with metronidazole treatment alone.
TV can be diagnosed in the laboratory by microscopic examination of a wet mount preparation, in vitro cultures and molecular methods. Our laboratory only uses wet mount microscopy for diagnosis. Urethritis is usually associated with a low concentration of organisms at site of the infection in males.8,9 The detection of TV by cytology in our case suggests a high load of TV at the site of infection, increasing the probability that Trichomonas might be playing an etiologic role. However, one cannot entirely rule out the possibility that an unidentified, metronidazole-responsive pathogen could have been involved.
CTC was a Canadian HIV Trials Network (CTN) and Royal College of Physicians and Surgeons of Canada Detweiler Traveling Fellowship recipient.
Krvavac S, 1990. Genitorectal Trichomonas invasion as (co)-factor in pathogenesis of Behcet's syndrome. Ann Rheum Dis 49: 423.
Arroyo R, Alderete JF, 1995. Two Trichomonas vaginalis surfaces proteinases bind to host epithelial cells and are related to levels of cytoadherence and cytotoxicity. Arch Med Res 26: 279–285.
Lubick KJ, Burgess DE, 2004. Purification and analysis of a phospholipase A2-like lytic factor of Trichomonas vaginalis. Infect Immun 72: 1284–1290.