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We report a case of perianal abscess due to Neisseria gonorrhoeae, which appears to have been suppressed but not eradicated by chronic low dose co-trimoxazole for a period of almost 6 months between acquisition and diagnosis.
The patient was a 34 year old HIV infected homosexual man treated with didanosine, stavudine, and nevirapine with a HIV viral load of 500 copies per ml and a CD4 lymphocyte count of 280 × 106/l. He was taking co-trimoxazole 400 mg/80 mg once daily to prevent Pneumocystis carinii pneumonia (PCP).
He reported last having receptive anal sex in June 2000. This was unprotected, with a casual partner at a “gay” sauna. Three weeks later he reported a perianal abscess which discharged spontaneously, requiring dressings for a few days. A sinus was observed and he was booked for elective surgery. He remained well for 5 months.
Co-trimoxazole PCP prophylaxis was stopped in November 2000 as his CD4 T lymphocyte count had remained above 200. Two weeks later (and almost 6 months after the last reported anal sex) he presented with purulent discharge emerging from a sinus approximately 3 cm from the anus.
N gonorrhoeae (sensitive to penicillin, ceftriaxone, and ciprofloxacin) and Bacteroides species were cultured from this discharge. Swabs from the rectum, throat, and urethra as well as urine were negative for N gonorrhoeae and Chlamydia trachomatis by polymerase chain reaction (PCR).
Oral ciprofloxacin was started but pain, swelling, and perianal cellulitis led to his admission to hospital where he was treated with intravenous ceftriaxone and metronidazole and surgical drainage.
Gonococcal perianal abscesses were reported in the pre-antibiotic era1 but have disappeared from contemporary descriptions of gonorrhoea, whereas Bartholin’s, periurethral, and tubo-ovarian gonococcal abscesses are described.2
The isolation of Bacteroides species and the worsening of the infection despite ciprofloxacin suggest that anaerobic organisms probably played a part in the development of an abscess, consistent with animal inoculation experiments.3 Another possible factor was the moderate immunosuppression (CD4 count of 280) from his HIV infection.
Six months passed from the time of infection to diagnosis, during which the patient was largely free of symptoms which then developed when co-trimoxazole was stopped. The likely explanation is that the co-trimoxazole was suppressing the gonococcal infection without curing it. The failure to detect N gonorrhoeae by PCR from the rectal specimen raises the possibility that co-trimoxazole may have eradicated a rectal infection in this case while only suppressing an extragenital manifestation.
It is now standard practice to stop PCP prophylaxis when CD4 counts rise above 200 × 106/l in patients taking antiretroviral therapy.4 This may in turn have some impact on both the transmission and the manifestations of gonorrhoea in these patients, perhaps even contributing to increases in gonorrhoea in HIV infected populations.5
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