The contamination of waterways by pathogenic microorganisms is, and remains, a threat to public health. The indicator organisms E. coli and Enterococcus are often used to signal the potential presence of pathogens in water. While it has been previously argued that growth of fecal bacteria and pathogens in secondary habitats is limited, there have been numerous reports documenting that suspended particles and sediments increase the survival time of bacteria in waterways, and that the survival of fecal indicator bacteria does not adequately mimic that of pathogens. Enteric pathogens such as enterohemorrhagic E. coli (EHEC), Salmonella, Shigella, and Campylobacter frequently cause diarrheal diseases in humans. Although Campylobacter was previously thought to survive poorly in the environment, C. jejuni has been isolated from soil, surface water, beach sand, and in waterborne protozoa. Likewise, while birds have been thought to be the major reservoir of Salmonella and Campylobacter, these pathogens have also been reported to exist outside their primary hosts, and E. coli O157:H7 has been detected in fresh vegetables, apple cider, and in manure-rich soils. Taken together, these results suggest that many secondary habitats provide conditions conducive for the growth and survival of fecal bacteria and pathogens once thought to be restricted to the gastrointestinal tracts of warm blooded animals. This has obvious public health implications. While current regulatory models and rules assume that waterborne fecal coliforms originate from humans, there is now accumulating data suggesting that wild and domesticated animals, and other non animal sources contribute to fecal loading of waterways. In this presentation I will discuss some of reasons why the environment harbors excessive levels of fecal bacteria, how non animal sources can contribute to the loading of waterways with fecal bacteria and pathogens, and the evolutionary factors that lead to these new input sources.