Rectal Lymphogranuloma Venereum, France

18.9) and also weakly associated with development of bloody diarrhea (OR = 2.5) (2). Avery uses the term endogeneity as it is used in econometric analyses; however, the term “intermediary variable,” i.e., a factor in the causal pathway leading from exposure to disease, is more frequently used in epidemiology. In this context, we chose to consider bloody diarrhea as a potential confounder (3). A confounder is a risk factor but is also independently associated with the exposure variable of interest and is not regarded as part of the causal pathway (see online Figure at http://www.cdc. gov/ ncidod/EID/vol 11no03/05-0071G.htm). Bloody diarrhea may act as a confounder if patients with bloody stools are treated differently by the examining physicians or if, for instance, unknown virulence factors contribute to the risk of having bloody stools. A second line of critique of our methods apparently develops from the idea that virulence factors determine the serogroup. This idea, however, is a biological misconception. In fact, virulence genes and serogroup are independent at the genetic level, and an important point of our article is that HUS is determined by the virulence gene composition of the strain rather than the serogroup. Regardless of the status of the bloody diarrhea variable, excluding it from the model doesn’t change the conclusions of the article. A revised model contains only the significant variables age and stx2 (Table). Serotype O157 is still not an independent predictor of HUS, and this result is robust.