Since the 1950s, numerous studies have examined the association between recreational water quality and health outcomes. Many of these studies have reported an increased risk of illness associated with exposure to recreational water. Several have related the level of contamination in the water, as measured by indicators of water quality, with the magnitude of risk. Despite extensive research on this topic, uncertainty remains about how water quality indicators can best be used in the regulation of recreational water environments. In 1986, the U.S. Environmental Protection Agency (U.S. EPA 1986) published recommended water quality criteria for recreational waters, which proposed the use of enterococci in marine water and enterococci and/or Escherichia coli in fresh water as indicator organisms. That report recommended regulatory levels based on geometric means of at least five samples over a 30-day period of 35 colony-forming units (cfu)/100 mL and 33 cfu/100 mL for enterococci in marine and fresh water, respectively; and 126 cfu/100 mL for E. coli in fresh water (U.S. EPA 1986). Fecal coliforms, which had been previously proposed for use as an indicator, were no longer recommended. The studies upon which these revised guidelines were based (Cabelli 1983;Dufour 1984a) have been criticized (Fleisher 1992), and the draft revised World Health Organization (2001) guidelines have been developed using more recent controlled studies ).Few attempts have been made to summarize and evaluate the existing literature in a systematic and quantitative framework. Pruss (1998) concluded that the literature strongly suggests a dose-response relationship between fecal contamination and the risk of gastrointestinal (GI) illness but did not examine the relationship between specific water quality indicators and health outcomes.Our primary goal in this systematic review was to evaluate the evidence linking specific microbial indicators of recreational water quality to specific health outcomes under nonoutbreak conditions. Secondary goals were to identify and describe critical study design issues, to quantify and evaluate sources of heterogeneity among the studies, and to evaluate the potential for health effects at or below the current suggested regulatory standards. MethodsLiterature search. Our literature search included several computerized databases: MEDLINE (http://www.ncbi.nlm.nih.gov/ entrez/query.fcgi?db=PubMed), BIOSIS (www.biosis.org), OLDMEDLINE (http:// gateway.nlm.nih.gov/gw/Cmd), and EMBASE (http://openaccess.dialog.com/med/) for the period from 1950 to the present. We searched dissertations using the UMI/ProQuest Digital Dissertation Database (http://wwwlib.umi.com/ dissertations/gateway). The search terms included key words "recreational water and health" and subject heading searches for "environmental pollutants, adverse effects" or "water pollution, adverse effects." We consulted experts in the field and reviewed the bibliographies of relevant studies for additional references. We reviewed the titles and abstracts of a...

On the basis of the evidence, we conclude that rotavirus responds to changes in climate in the tropics, with the highest number of infections found at the colder and drier times of the year.

SUMMARY The purpose of this study was to examine global epidemiological trends in human norovirus (NoV) outbreaks by transmission route and setting, and describe relationships between these characteristics, viral attack rates, and the occurrence of genogroup I (GI) or genogroup II (GII) strains in outbreaks. We analysed data from 902 RT-PCR-confirmed, human NoV outbreaks extracted from a systematic review of articles published from 1993 to 2011 and indexed under the terms “norovirus” and “outbreak.” Multivariate regression analyses demonstrated that foodservice and winter outbreaks were significantly associated with higher attack rates. Food- and waterborne outbreaks were associated with multiple strains (GI+GII). Waterborne outbreaks were significantly associated with GI strains, while healthcare-related and winter outbreaks were associated with GII strains. These results identify important trends for epidemic NoV detection, prevention, and control.

BackgroundDiscoveries that emerging and re-emerging pathogens have their origin in environmental change has created an urgent need to understand how these environmental changes impact disease burden. In this article we present a framework that provides a context from which to examine the relationship between environmental changes and disease transmission and a structure from which to unite disparate pieces of information from a variety of disciplines.MethodsThe framework integrates three interrelated characteristics of environment–disease relationships: a) Environmental change manifests in a complex web of ecologic and social factors that may ultimately impact disease; these factors are represented as those more distally related and those more proximally related to disease. b) Transmission dynamics of infectious pathogens mediate the effects that environmental changes have on disease. c) Disease burden is the outcome of the interplay between environmental change and the transmission cycle of a pathogen.ResultsTo put this framework into operation, we present a matrix formulation as a means to define important elements of this system and to summarize what is known and unknown about the these elements and their relationships. The framework explicitly expresses the problem at a systems level that goes beyond the traditional risk factor analysis used in public health, and the matrix provides a means to explicitly express the coupling of different system components.ConclusionThis coupling of environmental and disease transmission processes provides a much-needed construct for furthering our understanding of both specific and general relationships between environmental change and infectious disease.