Epidemiology of Anorectal Chlamydial and Gonococcal Infections Among Men Having Sex With Men in Seattle

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Abstract
Background Bacterial sexually transmitted diseases (STDs) among men who have sex with men (MSM) have recently increased in Seattle. Goals Serovar and auxotype typing of strains was used to assess the epidemiology of anorectal chlamydial and gonococcal infections among MSM attending an STD clinic. Study Design The prevalences of anorectal chlamydial infection and gonorrhea among MSM attending an STD clinic during the period of 1994 to 1996 were compared with prevalences during 1997 to 1999. A retrospective case–control study of MSM attending an STD clinic between 1997 and 1999 was performed. Anorectal chlamydial isolates were characterized by serovar and gonococcal isolates were characterized by serovar and auxotype. Infected MSM were mapped by residence and strain type. Results Prevalences of anorectal chlamydial and gonococcal infections increased from 4.0% and 6.3%, respectively, during 1994–1996 to 7.6% and 8.7%, respectively, during 1997–1999 (P = 0.004 and P = 0.013 for chlamydial infection and gonorrhea, respectively). Most chlamydial infections were caused by serovars G (47.9%) and D (29.6%), and most gonococcal infections were caused by auxotype/serovar classes Proto/IB-1 (43.3%), Proto/IB-3 (16.5%), and Proto/IB-2 (10.3%). MSM with anorectal chlamydial infection more often had chlamydial urethritis (P = 0.005) and were not white (P = 0.046), in comparison with controls. MSM with anorectal gonorrhea more often had pharyngeal gonorrhea (P < 0.001), had a history of gonorrhea (P = 0.003), and were younger than age 30 years (P = 0.039), in comparison with controls. Residences of MSM with anorectal gonorrhea were clustered in urban areas, whereas those of MSM with anorectal chlamydial infection were more dispersed. Conclusion Prevalences of anorectal chlamydial infection and gonorrhea among MSM in Seattle have increased dramatically over the past 3 years. Serovar and auxotype analyses indicate these increases are not clonal but are due to the spread of unique distributions of strains that differ from those causing urogenital infections in the same community.