Twenty-eight patients with genital and perianal necrotizing infections are described. The patients were divided into three groups according to the primary site of infection: group 1, anorectal (14 patients); group 2, urologic (ten patients), and group 3, idiopathic (four patients). The overall mortality was 25 percent, 28.5 percent for the anorectal group and 10 percent for the urologic group, although this difference is not statistically significant. Necrotizing infections of anorectal origin were more severe and had a less typical way of presentation, with subsequent delay in diagnosis and a higher rate of myonecrosis. As a consequence, more debridements and more fecal derivations had to be performed. The etiologic agents were the same among the three groups and comprised a number of anaerobes (Bacteroides spp, gram-positive cocci) as well as aerobes (microorganisms belonging to the Enterobacteriaceae and S. faecalis). Necrotizing fasciitis was the pathologic picture of nine of ten patients with Fournier's gangrene of urogenital origin and seven of 14 with an anorectal source. Synergistic necrotizing cellulitis was identified in half of those secondary to anorectal origin and only one of those with a urologic source.

In a prospective, multicentre, switch study to identify the most frequently occurring nucleoside reverse transcriptase inhibitor (NRTI)-associated toxicities that cause NRTI withdrawal in virologically suppressed HIV-infected patients, among those who underwent stavudine substitution by tenofovir, 271 had hypertriglyceridemia and 193 had hypercholesterolemia. After 12 weeks of switching from stavudine to tenofovir, triglyceride and cholesterol levels showed significant de-creases, which suggests that such a switch may reverse, at least partly, stavudine-associated dyslipidaemia.

Myeloradiculitis is a rare neurological complication of herpes simplex type 2 (HSV-2) infection, frequently associated with a fatal outcome. Among patients with HIV infection, HSV-2 myeloradiculitis has occasionally been reported, always associated with advanced immunosuppression and AIDS. We report a patient with HIV infection but no history of previous opportunistic infections, who developed sacral myeloradiculitis immediately after an episode of genital herpes. Magnetic resonance imaging with gadolinium showed necrotizing myelitis in the conus medullaris and enhancement of sacral roots. CD4 lymphocyte count was 530/mm3. Other possible causes of myeloradiculitis in HIV-infected patients were appropriately excluded. Acyclovir therapy resulted in partial clinical improvement. This report shows that myeloradiculitis as a complication of genital herpes may occur in the early stages of HIV infection and may have a favourable outcome with antiviral treatment.

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