Temporal trends in gonococcal population genetics in a high prevalence urban community

Abstract

Molecular evolutionary studies can provide insights into the spread of infectious diseases and inform infection control measures. We performed a population genetic analysis of gonococcal isolates obtained over a 15-year interval in Baltimore, MD, where gonorrhea is highly prevalent. Categorical analysis of genetic differentiation revealed temporal structuring of the gonococcal population. The use of a new method to determine the historical demography of Neisseria gonorrhoeae from sequence data showed a strong correlation with trends in the number of reported cases of N. gonorrhoeae. The historical trends may also reflect the influence of social and demographic factors and the impact of antimicrobial resistance on the molecular epidemiology of gonorrhea in Baltimore over the past 2 decades. The strong correlation between the population genetic inferences over the last 20 years and the demographic data collected over the same time period demonstrates the utility of these approaches for the accurate inference of complex population dynamics using multilocus sequence data. The real time application of population genetic analysis can provide sentinel data on gonococcal prevalence, antibiotic resistance patterns and changing epidemiology of gonococcal infections.

Figure 1

Reported cases of N. gonorrhoeae in Baltimore and genetic population size from 1970 to 2004. The red line shows the number of reported N. gonorrhoeae cases. Relative genetic population size (Neτ) was estimated from housekeeping genes (black lines), fluoroquinolone resistance genes (green lines) and porB gene (blue lines), with the solid line showing the mean estimate and the dashed lines the 95% highest posterior density (HPD) limits.

Figure 2

N. gonorrhoeae population dynamics during the 120 years preceding 2005 derived from isolates sampled in Baltimore in 1991, 1996, 2001 and 2005. Relative genetic population size (Neτ) was estimated from 7 housekeeping genes (black lines), the fluoroquinolone resistance genes gyrA and parC (green lines) and the porB gene (blue lines), with the solid line showing the mean estimate and the dashed lines the 95% HPD limits.