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Indicators for Waterborne Pathogens 3 Ecology and Evolution of Waterborne Pathogens and Indicator Organisms INTRODUCTION Past efforts to develop and implement indicators of waterborne pathogens have often given little or no consideration to the role of evolution in the ecology and natural history of waterborne pathogens of public health concern. Evolution is a powerful force and can act quickly, even over ecological timeframes, to bring about change in pathogenic and indicator microorganisms. Furthermore, although numerous studies exist on the pathogenicity of various waterborne pathogens few have sought to describe their life history or ecology. The interactions between pathogens and their hosts involve complex and diverse processes at the genetic, biochemical, phenotypic, population, and community levels, while the distribution and abundance of microorganisms in nature and their microbial processes are affected by both biotic and abiotic factors that act at different scales. To develop new and more effective indicators of waterborne pathogens it is important to better understand how both evolution and ecology interact with the genomes and natural history of waterborne pathogens and their indicators, if different from themselves. Failure to consider these effects may result in spurious conclusions that do not truly reflect the abundance and distribution of waterborne pathogens. Most of the waterborne pathogens discussed in this report (see also Appendix A) are not native to the types of waterbodies addressed herein. Notable exceptions include various species of Vibrio and Legionella bacteria and protozoan parasites such as the free-living amoebae Naegleria and Acanthamoeba. Many microorganisms that are pathogenic to humans and animals enter ambient waters after import from various point and diffuse sources. Upon entry, new selective
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Indicators for Waterborne Pathogens BOX 3-1 Summary of Important Ecological and Evolutionary Questions That May Affect the Understanding of Various Indicators for Waterborne Pathogens and Infectious Diseases What is the distribution and abundance of waterborne pathogens? Are these environmental reservoirs of pathogens biotic or abiotic? What are the fates of freshwater pathogens when imported into marine or brackish waters? Is the residence time of a pathogen sufficient to allow genetic exchange or change to occur? What biotic and abiotic factors influence the viability and survivability of waterborne pathogens? Are there environmental conditions that promote genetic exchange or the acquisition of genetic elements that confer selective advantage under clinical conditions? What effect do sampling and environmental variations have on the efficacy of indicators? forces begin to act on these introduced or exotic microorganisms, whether eukaryotes or prokaryotes. This chapter describes basic principles of ecology and evolution for waterborne viruses, bacteria, and protozoa (and yeasts and molds to a lesser extent) of public health concern as an aid to better understand how selective forces may alter one’s ability to assess the microbial quality of water. Indeed, indicators of microbial water quality can be the pathogenic organisms themselves, other microorganisms, or other physical or chemical aspects of the aquatic environment (see Chapter 4 for further information), and any biological indicator is subject to evolutionary and ecological changes. The final section is a summary of the chapter and its conclusions and recommendations. Answers to several sets of related and fundamental questions (summarized in Box 3-1) are imperative to facilitate the understanding of indicators of waterborne pathogens and emerging infectious diseases. These questions include but are not limited to the following: What is the natural distribution and abundance of waterborne pathogens? Are there environmental reservoirs of these microorganisms and, if so, what environmental conditions promote their maintenance or growth? Are these environmental reservoirs biotic or abiotic (i.e., from the living or nonliving)? Can waterborne pathogens colonize and proliferate in sediments or within aquatic systems? The concepts of growth and regrowth are most often applied to water distribution systems and wastewater discharges (and their receiving waters), respectively.
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Indicators for Waterborne Pathogens Determining whether and how survival and growth occur under natural conditions is important in understanding whether an indicator is indicating “new” contamination. The ecological concept of “source/sink” (Pulliam and Danielson, 1991) needs to be better understood for waterborne pathogens. Are there populations of pathogens or indicator organisms in the environment (sources) that continually feed other habitats where the pathogens or indicators can be found (often at high densities) but cannot grow (sinks)? What is the fate of freshwater pathogens that are transported into brackish or marine habitats and vice versa? The transition from fresh- to saltwater or the reverse is physiologically demanding, and microbial assemblages change both phenotypically and phylogenetically along salinity gradients. Given that freshwater has been imported into U.S. coastal waters for hundreds of years, along with the propensity of microbes to survive in novel environments, some freshwater pathogens might have adapted to increased salinity and some seawater pathogens might have adapted to reduced salinity. If so, flushes of these now “naturally” occurring bacteria may not be indicative of new inputs from either storms or saltwater intrusion but rather indicative of in situ bacterial growth. Is the residence time of waterborne pathogens and indicators within a body of water sufficient for evolutionary mechanisms to alter the genetic composition of the pathogens? If so, could the genetic changes confound the reliability of the indicators or indicator mechanisms? Before selection can alter the genetics of a microorganism, the selective force must be applied for sufficient time and under the right conditions. Imported pathogens or pathogen indicator species gain or lose genetic traits under natural conditions—traits that may be the basis for detecting various indicators (e.g., β-galactosidase activity). What biotic and abiotic factors influence the viability and survivability of waterborne pathogens and their indicators? Are there environmental conditions that promote genetic exchange or the acquisition of genetic elements that confer selective advantage under clinical conditions? For example, the increases in antibiotic and multiple antibiotic resistances may be influenced by physical conditions in the environment. What is the frequency of genetic exchange among native bacteria and introduced or imported bacteria? What are the effects of sampling regime and environmental variation on the efficacy of indicators (see also Chapters 4 and 5)? Population, community, or genetic changes in space or time increase variability. Measures of statistical central tendency (i.e., means, medians, modes) are important in many aspects of science and ecology. However, because exposures at high extremes pose the greatest human health risks—and because of the immense economic component associated with waterborne pathogens and especially outbreaks (see also Chapter 2), including recreational losses and clinical costs—knowledge of simple means, medians, or modes is insufficient for making informed decisions about human health risks. Environmental variability occurs both spatially and temporally, and to understand ecological phenomena such variance must be estimated.
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Indicators for Waterborne Pathogens Many human pathogens and candidate indicators of fecal contamination also infect other host animals. Thus, nonhuman hosts may be the natural reservoirs of human pathogens and indicators. These additional ecological niches of pathogens and indicators have major implications for the following: the potential detection, load estimation, and tracking of fecal contamination sources; the ability to distinguish among and track or trace microbes of the same genus and species but from different sources; the ability of pathogens from different sources to cause infection and illness; and the potential for genetic exchange and evolution in microorganisms by coinfection of different strains or genotypes in a host animal or human or in the environment. Identification of specific sources of pathogens or indicators is impossible unless advanced analytical methods, such as those described in Chapters 4 and 5, are used to genetically or phenotypically characterize the microorganisms. Because the same species of microorganism from different animal hosts or environmental reservoirs can differ greatly in human infectivity and the ability to cause disease, determining risks to human health requires the use of advanced analytical methods that are often well beyond the methods currently used for their detection in environmental waters. Furthermore, the continuous movement of microorganisms through different hosts and abiotic environmental media exerts selective pressures that are opportunities for genetic change leading to the emergence of new strains with different traits and health risks. Current analytical methods used to detect and quantify pathogenic and indicator microbes in water are limited in their ability to distinguish among genetically and phenotypically different organisms and to determine their sources or their human health risks. Effects of Environmental Change Environmental change at all scales, from local to global, influences microbial populations and indicator organisms. Large-scale or global changes in weather or climate are predicted to have major effects on waterborne or vectorborne diseases (Patz and Reisen, 2001; Patz et al., 2000). Past and continued alteration of forested areas (e.g., deforestation) and natural waters (e.g., water diversions such as dams and drainages of lakes, river diversions), road construction, commercial and residential development, and other disturbances change the ecological conditions of waterways. These changes often favor introduced over indigenous or “native” organisms at all levels of biological organization and can also result in changes in microbial diversity, the introduction of new or increased levels of pathogens and indicator organisms, and increased opportunities for hu-
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Indicators for Waterborne Pathogens BOX 3-2 The Cholera Paradigm Colwell (1996) described the appearance of a new serogroup of Vibrio cholerae 0139 in 1992 in India. Cholera has had at least seven pandemics since 1817. This disease often disappears for decades and then reemerges with a vengeance. From 1926 to 1960, cholera was expected never to reach pandemic proportions because of the improvement in water supplies worldwide. Yet nature prevails, and in 1961 a new pandemic began and continues to this day. The responsible biotype of V. cholerae was designated El Tor 01. This particular biotype does not cause as severe disease as the classical type. However, in 1992 a new serogroup 0139 emerged in India. Evidence suggests that the new serogroup originates from genetic recombination, horizontal gene transfer, and subsequent acquisition of unique DNA. Furthermore, this new serogroup had completely replaced the V. cholerae 01 in Calcutta by 1993. Various environmental factors have been implicated in the evolution of a new serogroup. The combination of increased inputs of nutrients to eutrophic conditions and association of the organism with shellfish, fish, and zooplankton created environmental reservoirs that could persist for extended periods of time. Thus, reintroduction was not necessary. The association with zooplankton, especially copepods, is central to understanding the dispersal and distribution of cholera. Vibrio cholerae preferentially attach to the chitinous exoskeleton of the copepods and thereby have the potential to be transported with ocean currents. man exposure to native pathogens of that environment via water and other routes. Therefore, increases in disease-causing microorganisms would be predicted (see Box 3-2). For example, certain aquatic ecosystem restoration projects that require construction of wetlands by legislation may affect the growth and distribution of waterborne pathogens. Lake inflows are controlled, in part, by littoral zones or lake margins, and such areas can greatly impact the thermal mediation of small or forested watersheds. Andradottir and Nepf (2000) suggested that littoral wetlands can actually raise the temperature of inflow during the summer and create surface intrusions rather than plunging inflows. In other words, density differences between surface and underlying water would cause warm water to flow above the cooler layers. Consequently, nutrients, contaminants, and pathogens that were previously in the underlying water enter the surface layer, thereby increasing the risk of human exposure in recreational water settings. Furthermore, warmer, nutrient-rich waters may favor growth of pathogens.
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Indicators for Waterborne Pathogens Lebaron et al. (1999) have shown that varying nutrient conditions in seawater affect bacterial communities directly and indirectly by stimulating either bacteria or various protozoans that selectively feed on the bacterial assemblage. The stimulation of protozoan fauna may be acute given their interaction with various pathogens (discussed later). In relatively simple mesocosms, bacterial assemblages could be affected by nutrient additions that promote increased growth and productivity. In complex environments, numerous and varied microhabitats (such as organic foams which are described later) exist that may provide the appropriate conditions for changes in microbial assemblages through either direct or indirect selection. Implications for Indicators The concept of indicators implies that certain characteristics of an organism (e.g., genes or gene products) are constant under varying environmental conditions. This major assumption is questionable and subject to verification. Although various (primarily bacterial) indicators have been historically effective in detecting and quantifying fecal contamination, they are not always reliable predictors of microbial water quality due largely to our lack of understanding of the basic ecology of waterborne pathogens and indicators. For example, total coliform counts and enterococci have been used as indicators of human fecal contamination for decades (see Chapter 1). However, there are nonhuman and naturally occurring coliforms and enterococci, and their presence confounds the results of the total coliform and enterococci tests. All coliforms and enterococci do not have the same ecology. If one or more species of coliforms and enterococci had different biotic and abiotic sources and greater or lesser survivability than the indicator species or pathogen of concern, then their presence or absence would not be a reliable indicator of the source or survivability of that pathogen. Similarly, the use of E. coli as an indicator of human fecal contamination in areas where there are high numbers of naturally occurring or introduced E. coli would greatly overestimate a potential microbial contamination problem. Not recognizing alternative sources of indicator organisms could ignore their potential to detect and correctly characterize actual waterborne microbial contamination problems. More specifically, wastewater treatment processes, physical and chemical stressors, and biological antagonists, such as naturally occurring predators, can selectively affect the presence and survival of one “indicator” species, which in turn affects the implied correlation between the indicator and the target pathogen. Furthermore, gene products such as β-galactosidase or β-glucuronidase may not be produced or may be overproduced under various environmental conditions, thereby affecting indicator technologies based on the detection and quantification of these products. Microbial species can change genetically under natural conditions in ways that can alter their ability to be detected by phenotypic or genotypic methods.
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Indicators for Waterborne Pathogens Some of these changes can be profound, with genomes increasing or decreasing in actual DNA content and changing phenotypic properties. Bacteria in aquatic systems have been shown to take up plasmids at fairly high rates. Fry and Day (1990) demonstrated that maximum uptake occurs within 24 hours but that transconjugants could be detected within the first three hours of their experiments. Recently, high mutation rates have been observed in stationary phase E. coli from various natural habitats (Loewe et al., 2003) and stressed aging colonies have also been shown to have increased mutagenesis (Bjedov et al., 2003). Both of these responses could result in increased adaptive responses and emergence of pathogenicity (Loewe et al., 2003). Notably, all of these mechanisms were shown to occur within 24 hours. In natural systems the residence times of introduced bacteria can be much longer than 24 hours, thus providing an opportunity for genetic changes either through acquisition of plasmids or by allowing mutations to take place under the selective pressures of the new habitat. Various natural history and environmental aspects of pathogens and indicator organisms also contribute to their ability to be detected and monitored. Many of these aspects are discussed below because they directly relate to the ongoing public health challenge of developing and using better indicators for waterborne pathogenic viruses, bacteria, certain parasitic protozoa, and to a lesser extent—yeasts and molds. VIRUSES Introduction to Viruses and Their Properties Virus-host interactions are fundamental to the biology and ecology of viruses because they are obligate intracellular parasites. Viruses are inert outside host cells, despite their persistence in the environment and their ability to infect another host when the opportunity arises. In this section, the ecology and evolution of viruses are considered, particularly for waterborne viruses that are human and animal pathogens or bacterial viruses that are potential indicators of fecal contamination. Virus Composition, Basic Properties, and Diversity Viruses are among the smallest and simplest microbes and are obligate intracellular parasites of host cells. They range from about 0.02 to 0.1 μm in size and consist of a nucleic acid surrounded by a protein coat or capsid. The capsid not only is protective but also functions as the structure for host cell attachment leading to infection, because it has specific chemical structures that recognize receptor sites on the host cell. Some viruses, although usually not the ones transmitted by fecally contaminated water, also possess an outermost lipoprotein membrane called the envelope. The envelope is usually a virus-modified host cell membrane
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Indicators for Waterborne Pathogens containing virus-specific glycoproteins that is acquired as the virus exits the cell. Some of these glycoproteins in enveloped viruses are the chemical structures for attachment to host cell receptors. Viruses contain relatively small amounts of nucleic acid, usually from a few to several tens of nucleotide kilobases—enough information to encode a few to several tens of proteins. Despite this relative paucity of genetic information, viruses are genetically diverse, sometimes highly genetically variable, and quite capable of adapting to the changing conditions of their host cells and the host environment. Viral Replication, Virus-Host Interactions, and Viral Evolution The replication and evolution of viruses and their interactions with their hosts are strongly related to host fitness as both viruses and hosts coevolve. The ability of a virus to infect a particular host cell is primarily a function of the availability of the appropriate chemical structures on the surface of the virus and the host cell that allow for attachment to and penetration of the cell. These receptor-dependent interactions determine the virus host range, tissue tropisms (i.e., ability to infect cells of a particular tissue, such as intestinal, liver, or neurological tissues) for human and animal hosts, and thus the ability to cause certain kinds of infections and diseases. Despite the importance of cell surface receptors in the susceptibility of different cells or tissues to viral infection, the outcomes of viral infection—especially disease—are often mediated by additional events and other molecular interactions during virus replication (Bergelson, 2003; Dimitrov, 2000; Jindrak and Grubhoffer, 1999; McFadden, 1996; Mims et al., 2001; Ohka and Nomoto, 2001; Tyler and Nathanson, 2001). Several outcomes of viral infection of host cells are possible: (1) virus multiplication leading to many progeny viruses with resulting cell lysis and death; (2) virus multiplication leading to many progeny viruses but cell survival; and (3) development of a stable relationship (at least temporarily) with the host cell with little or no virus multiplication—either as a discrete intracellular genetic element or as an integrated part of the host cell’s genetic material. In the last situation, the virus genetic information is propagated as part of the cell when it divides, and a relationship of co-existence between the cell and the viral genome may form (lysogeny). Under some circumstances, however, the virus genetic material can become capable of initiating replication activities of the viral genome, leading to the production of progeny viruses, lysis, and death of the cell (the lytic cycle). In some cases, the course of the alternative events in viral infection and virus-host interaction, lysogeny (or integration) or the lytic (or cytopathogenic) cycle, are influenced by a number of virus, host, and environmental factors, such as temperature, pH, UV irradiation (sunlight), nutrients, and antagonists (toxicants). At the human or animal host level, factors influencing the activation of latent viruses to a more active cytopathogenic cycle of events in virus infection and disease can include immune status, hormone levels, chemical (nutritional) cofac-
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Indicators for Waterborne Pathogens tors, age, gender, and pregnancy. Therefore, the potential for, or likelihood of, viral infection and the potential outcomes of viral infection are complex and not easily predicted. In fact, some of the most studied viruses (e.g., hepatitis) are still not well understood, making reliable predictions of viral infection and disease outcomes at either the cellular or the population level difficult, if not impossible. Despite the variability and uncertainty of predicting waterborne virus infection and disease outcomes, studies of virus properties, virus-host interactions, virus infection and disease outcomes, and viral ecology and epidemiology have all helped to elucidate the natural history of viruses and virus risks to their hosts. Virus strains that produce infectious viruses more rapidly and at higher yield are more likely to be successful if fitness is positively correlated with population size of the susceptible host. For many viruses the manifestation of disease in the host is rare, and most infections are unapparent or subclinical. Examples of such viruses are the polioviruses and the rotaviruses. Typically, these viruses infect the youngest members of the population who have previously not been infected. Unfortunately, such infections produce severe disease or death in a small proportion of the humans they infect, and the majority of infections in infants and young children are either subclinical (polioviruses) or mild and self-limiting (rotaviruses). However, the consequences of poliovirus infection are considered sufficiently profound in the small proportion of infected persons who develop paralytic disease or die that vaccination is considered essential and a global eradication for polio is under way by the World Health Organization (Hull and Aylward, 2001). Repeated rotavirus infections are common in infants and young children though most infections are not life-threatening, especially in healthy children in developed countries. However, rotavirus diarrhea does cause severe disease requiring hospitalization in a low proportion of infected infants and children in the United States and other developed countries (<1 percent of rotavirus infections) and there is a very low but non-zero risk of death from rotavirus infections (Parashar et al., 2003). Hosts that recover from virus infections are immune to future infections, either temporarily or perhaps indefinitely. In the case of rotaviruses, immunity is transient, only partially protective, and even less protective against antigenically different rotaviruses that have considerable antigenic diversity (Jiang et al., 2002). In the case of polioviruses, infection is likely to result in long-lasting immunity that is protective against paralytic disease and mortality, although enteric infections that are subclinical or mild still occur in persons with immunity (Ghendon and Robertson, 1994). If primary (initial) poliovirus infection of a susceptible host does not occur until later in life, as an older child or an adult, the consequences of infection are likely to be severe disease or even death. For polioviruses, infection of infants and children is common in developing countries where poor sanitation and hygiene result in exposure early in life. However, in developed countries with improved hygiene and sanitation, virus exposure often does not occur until later in life so that the likelihood of severe disease and death as a
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Indicators for Waterborne Pathogens result of infection is much greater (Evans, 1989; Pallansch and Roos, 2001; White and Fenner, 1994). The above examples serve to highlight the importance of host status and environmental conditions in the ecology and natural history of viruses, and to demonstrate that the “virulence” or pathophysiology of a virus depends on the status of the host and its environment. Another example of the role of the host and its environment in the outcome of virus infection is hepatitis E virus (HEV). In developing countries, the members of the population at highest risk of severe illness and death are pregnant women. The mortality rate in this group can be as high as 25 percent (Aggarwal and Naik, 1997; Balayan, 1997; Emerson and Purcell, 2003; Hyams, 2002; Krawczynski et al., 2001). Yet, for most of the population in developing countries, HEV infection apparently occurs relatively early in life, with little illness incurred. Children are often asymptomatic and the mortality rate is between 0.1 and 4 percent (Grabow et al., 1994). Seroprevalence of HEV in developing countries ranges from 5 to upwards of 20 percent (Kamel et al., 1995; Mohanavalli, 2003). In developed countries such as the United States, HEV infection is rare and results in very few cases of disease (most traced to probable virus exposures in developing countries); seroprevalence is less than 5 percent (Bernal et al., 1996; Redlinger et al., 1998). Therefore, as with many other viruses, the pathophysiology of HEV varies with the health status of the host and with environmental conditions. Viral Genetic Variability and Genetic Change Viruses have evolved a variety of mechanisms that influence their host interactions and their ability to persist over time and in space. Viruses mutate spontaneously and without direct exposure to physical and chemical mutagens during replication in host cells. Mutation rates vary among different virus groups from high rates of 10–3 to 10–4 per incorporated nucleotide in the single-stranded RNA viruses to rates as low as 10–8 to 10–11 per incorporated nucleotide in some of the double-stranded DNA viruses (Domingo et al., 1999). Genetic changes in viruses that involve relatively minor substitutions, insertions, or deletions of nucleotides as point or frameshift mutations can occur. Such changes are often referred to as genetic drifts, and if they occur in an expressed gene these changes are referred to as antigenic drift. Genetic and antigenic drifts can occur in response to selective pressures from host populations, such as immunity and genetic changes in host cells and whole hosts such as animals and plants. In some cases, genetic drift leads to more benign relationships between viruses and their hosts. At the other extreme, it can result in viruses with properties that have severe consequences, such as the reversion of attenuated poliovirus vaccine strains to a neurovirulence and the ability to cause paralytic disease in human hosts.
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Indicators for Waterborne Pathogens Effects of Virus Mutation on Hosts: Poliovirus Virulence, Attenuation, and Reversion to Virulence Polioviruses are single-stranded RNA viruses belonging to the Picornaviridae family and the Enterovirus genus, and they consist of three genetically distinct types (I, II, and III). These viruses infect the gastrointestinal tract initially and can then spread via the bloodstream and lymphatic system to the central nervous system, thereby causing paralysis in their human hosts. The virus-specific factors responsible for the neurovirulence of polioviruses are still not fully understood at the genetic, protein, or virion (whole virus particle) level. Neurovirulence is mediated by the ability of the virus to successfully infect neurons and cause high levels of virus production and subsequently death of these cells (Ohka and Nomoto, 2001; Pallansch and Roos, 2001; Racaniello, 2001). Paralytic disease depends on the ability of the virus to infect cells of the central nervous system efficiently. The risks of paralytic disease to humans posed by wild-type, neurovirulent polioviruses, led to the selection of avirulent or attenuated polioviruses as vaccine strains in the mid-twentieth century. These live oral poliovirus vaccine strains differ from wild-type viruses because they have several different point mutations that are associated with the ability to infect neural cells. However, despite thorough knowledge of the complete nucleotide sequence of polioviruses for two decades, the cloning and expression of the cell surface receptor of the virus, the development and use of a transgenic (genetically modified) mouse model for neurovirulence, and considerable effort to identify neurovirulence mechanisms in cell culture and animal systems, these mechanisms have not been fully elucidated. However, it is becoming clear that neurovirulence depends on host factors as much as virus-specific factors and that virus-host interactions leading to neurovirulence are probably modulated by the host (Ohka and Nomoto, 2001; Yoneyama et al., 2001). The attenuated live oral vaccine strains of poliovirus are also subject to back-mutations that cause reversion to wild-type viruses and paralytic poliomyelitis in vaccine recipients. Because virus mutation rates are high, there is rapid reversion of vaccine polioviruses to genotypes with neurovirulent properties among the excreted viruses of vaccine recipients. Serial transmission of vaccine strains of polioviruses among susceptible human hosts results in the accumulation of mutations, which can eventually lead to selection and further serial transmission of neurovirulent vaccine strains. This highly unfortunate outcome occurs when there is inadequate vaccine coverage of susceptible hosts over time, as occurred recently in the Dominican Republic and Haiti on the island of Hispaniola, the Philippines, and several other locations globally (Anonymous, 2002, 2003; Friedrich, 2000; Landaverde et al., 2001). Based on the extent of genetic change (about one to three percent), these viruses had apparently been spreading from person to person over one to two years or more.
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Indicators for Waterborne Pathogens the infectivity and pathogenicity of the organism. Therefore, additional research is needed on microbial evolutionary ecology to address long-term public health issues. The ecology of waterborne pathogens should be assessed in relation to modern agricultural practices and other anthropogenic activities, such as urbanization. Animal wastes from agriculture and urban sewage, runoff, and stormwater are major contributors to both human pathogenic and nonpathogenic strains of microbes, and the wide use of antibiotics in animal agriculture and in human and veterinary therapy leads to selection for antibiotic-resistant phenotypes. Research in genetic ecology is needed to address issues of bacterial resistance to antibiotics, disinfectants, and other chemicals (such as heavy metals) and the regulation and transferability of these resistance traits either independently or together as sets of multiple resistance genes. The factors that select for increased resistance to these agents in natural populations of bacteria need to be elucidated as do the factors influencing the natural transfer of these resistance traits to waterborne pathogens, indicators, and other aquatic microorganisms. Research is needed to develop a better understanding of the ecology and natural history of both the environmental and infectious stages of pathogens and the parallel stages of indicator organisms to grasp how the organisms are distributed in nature; how they persist and accumulate in water, other environmental media, and in animal reservoirs; and how dissemination of the environmental form occurs, especially human exposures. Genetic and phenotypic characterization of pathogenic viral, bacterial, and protozoan parasites is needed to elucidate zoonotic relationships with their hosts and factors influencing waterborne transmission to humans. Given the ubiquity of yeasts and molds in water samples, research should be conducted to clarify their role in the transmission of waterborne diseases. REFERENCES Aggarwal, R., and S.R. Naik. 1997. Epidemiology of hepatitis E: Past, present and future. Tropical Gastroenterology 18: 49-56. Alexopoulos, C.J., C.W. Mims, and M. Blackwell. 1996. Introductory Mycology. New York: John Wiley and Sons. Ali, S.A., and D.R. Hill. 2003. Giardia intestinalis. Current Opinion in Infectious Diseases 16(5): 453-460. Allen, R.D. 1987. The microtubulues as an intracellular engine. Scientific American 256: 42-49. Anderson, O.R. 1988. Comparative Protozoology: Ecology, Physiology, Life History. New York: Springer-Verlag. Andradottir, H.O., and H.M. Nepf. 2000. Thermal mediation by littoral wetlands and impact on lake intrusion depth. Water Resources Research 36: 725-735. Anonymous. 2002. From the Centers for Disease Control and Prevention. Acute flaccid paralysis associated with circulating vaccine-derived poliovirus - Philippines, 2001. Journal of the American Medical Association 287(3): 311. Anonymous. 2003. Laboratory surveillance for wild and vaccine-derived polioviruses, January 2002-June 2003. MMWR 52(38): 913-916.
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