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Global Issues in Water, Sanitation, and Health: Workshop Summary 2 Lessons from Waterborne Disease Outbreaks OVERVIEW This chapter is comprised of three case studies of waterborne disease outbreaks that occurred in the Americas. Each contribution features an outbreak chronology, an analysis of contributing factors, and a consideration of lessons learned. Together, they illustrate how an intricate web of factors—including climate and weather, human demographics, land use, and infrastructure—contribute to outbreaks of waterborne infectious disease. The chapter begins with an account of the massive cholera epidemic that began in urban areas of Peru in 1991 and swept across South America by Carlos Seas and workshop presenter and Forum member Eduardo Gotuzzo, of Universidad Peruana Cayetano Heredia and Hospital Nacional Cayetano Heredia in Lima, Peru. The authors describe current understanding of the role of Vibrio cholerae in marine ecosystems, and consider how climatic and environmental factors, as well as international trade, may have influenced the reintroduction of this pathogen to the continent after nearly a century’s absence. The epidemic persisted for five years, then reappeared, with diminshed intensity, in 1998. While attempts to control the epidemic through educational campaigns aimed at improving sanitation were unsuccessful in the short term, Seas and Gotuzzo report that, following a significant investment in sanitation in the wake of this public health disaster, transmission rates of other waterborne infectious diseases, including typhoid fever, declined in Peru. They note that, by understanding the ecology of V. cholerae, researchers may be able to predict relative risk for pathogen transmission from marine environments and thereby aid efforts at preventing epidemics.
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Global Issues in Water, Sanitation, and Health: Workshop Summary In 1993, two years after cholera struck Peru, an epidemic of cryptosporidiosis in Miluwaukee, Wisconsin, sickened hundreds of thousands of people and caused at least 50 deaths, demonstrating that even “modern” water treatment and distribution facilities are vulnerable to contamination by infectious pathogens. In their contribution to this chapter, workshop presenter Jeffrey Davis and coauthors recount their investigation of this outbreak, which resulted from the confluence of multiple and diverse environmental and human factors. Based on lessons learned from their discoveries, the authors made—and authorities undertook—recommendations to prevent further outbreaks in the Milwaukee water system, resulting in significant improvements in water quality. Their findings have proven applicable to other water treatment facilities that share Lake Michigan and have received attention from water authorities worldwide. The final paper in this chapter, by workshop presenter Steve Hrudey and Elizabeth Hrudey of the University of Alberta, Canada, discusses an episode of bacteria contamination of the water in Walkerton, Ontario, in 2000. The outbreak sickened nearly half of the town’s 5,000 residents and caused 7 deaths, as well as 27 cases of hemolytic uremic syndrome, a severe kidney disease. Several incidents of human error and duplicity figure prominently among the causes of this entirely preventable outbreak, the authors explain. “Because outbreaks of disease caused by drinking water remain comparatively rare in North America,” they conclude, “complacency about the dangers of waterborne pathogens can easily occur.” Based on their findings, they present a framework for water system oversight intended to save other communities from Walkerton’s fate. THE CHOLERA EPIDEMIC IN PERU AND LATIN AMERICA IN 1991: THE ROLE OF WATER IN THE ORIGIN AND SPREAD OF THE EPIDEMIC Carlos Seas, M.D.1 Universidad Peruana Cayetano Heredia Eduardo Gotuzzo, M.D., FACP1,2 Universidad Peruana Cayetano Heredia At Athens a man was seized with cholera. He vomited, and was purged and was in pain, and neither the vomiting nor the purging could be stopped; and his voice failed him, and he could not be moved from his 1 Insitituto de Medicina Tropical Alexander von Humboldt. Universidad Peruana Cayetano Heredia, Lima, Peru, and Departamento de Enfermedades Infecciosas, Tropicales y Dermatológicas. Hospital Nacional Cayetano Heredia. Lima, Peru. 2 Corresponding author. Av. Honorio Delgado 430, Lima 31, Peru. Phone: 51-1-4823910, Fax: 51-1-4823404, E-mail: firstname.lastname@example.org.
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Global Issues in Water, Sanitation, and Health: Workshop Summary bed, and his eyes were dark and hollow, and spasms from the stomach held him, and hiccup from the bowels. He was forced to drink, and the two (vomiting and purging) were stopped, but he became cold. Hippocrates After an absence of almost one century, cholera reappeared in South America in Peru during the summer of 1991. This event was totally unexpected by the scientific community, which had anticipated the spread of cholera to the continent from Africa and had hypothesized its introduction by Brazil following well-recognized routes of dissemination of the disease that involve trade and commerce. The further spread of the epidemic was very rapid; all Peruvian departments had reported cholera cases in less than six months; almost all Latin American countries, with the exception of Uruguay, had reported cases within one year of the beginning of the epidemic. The chains of events that triggered and disseminated the epidemic into the continent have not been fully elucidated, but evidence is being gathered on the possible role of marine ecosystems, climate and environmental factors, and the pivotal role of water. We discuss here the evidence in support of water’s role in cholera dynamics. The Environmental Life Cycle of Vibrio cholerae The natural reservoirs of V. cholerae are aquatic environments, where O1 and non-O1 serogroups coexist. V. cholerae survives by attaching to and forming symbiotic associations with algae or crustacean shells (Figure 2-1). In these environments, V. cholerae multiplies and can persist for years in a free-living cycle without human intervention, as it has been elegantly described by Dr. Colwell and her associates at the International Centre for Diarrheal Diseases Research in Dhaka, Bangladesh (Colwell et al., 1990). A number of environmental factors modulate the abundance of Vibrio, including, but not limited to, temperature, pH, salinity, and nutrient availability. Under adverse conditions, V. cholerae survives in a dormant state with all metabolic pathways shut down, which can be reactivated again when suitable conditions return. Additionally, V. cholerae can produce biofilms—surface-associated communities of bacteria with enhanced survival under negative conditions—which can switch to active bacteria and induce epidemics. The ability of V. cholerae to regulate its metabolism based on the environmental conditions of its natural reservoir may explain the endemicity of cholera in many parts of the world. During the cholera epidemic in Peru, V. cholerae was isolated from many aquatic environments, including not only marine ecosystems, but riverine and lake environments. Even one of the highest commercially navigable freshwater lakes in the world, Lake Titicaca, located 3,827 meters above sea level on the border of Peru and Bolivia, was impacted by the cholera epidemic of 1991.
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Global Issues in Water, Sanitation, and Health: Workshop Summary FIGURE 2-1 Vibrio cholerae O1 attached to a copepod. SOURCE: Courtesy of Rita Colwell, Ph.D., University of Maryland. Humans are only temporary reservoirs of V. cholerae. Interestingly, lytic phages modulate the abundance of V. cholerae in the human intestine, but on the other hand, V. cholerae are able to up-regulate certain genes in the intestine of humans resulting in a short-time hyperinfectious state. As illustrated in Figure 2-2, V. cholerae is introduced to humans from its aquatic environment through contamination of food and water sources. The Origins of the Latin American Epidemic The Latin American cholera epidemic was officially declared in Peru during the third week of January 1991, almost simultaneously in three cities along the north coastal area of the country. By the end of that year, almost 320,000 cases had been officially reported to the Pan American Health Organization by the Peruvian Ministry of Health. Nearly 45,000 cases occurred every week, in what was considered the worst cholera epidemic of the century in Peru (Gotuzzo et al., 1994). There were several distinctive features of this epidemic: Very high attack rates were reported soon after the epidemic started.
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Global Issues in Water, Sanitation, and Health: Workshop Summary FIGURE 2-2 A hierarchical model for cholera transmission. SOURCE: Reprinted from Lipp et al. (2002) with permission from the American Society for Microbiology. Cholera accounted for almost 80 percent of all acute diarrhea cases in the country irrespective of the degree of dehydration and age group. The epidemic was initially concentrated in urban areas, where it spread very rapidly, suggesting a common source of dissemination. Transmission was halted in very few areas, where treatment and chlorination of municipal water was possible, suggesting a critical role of water in the transmission of the disease. Very low case-fatality rates were reported from urban areas where patients had access to treatment by well-trained health personnel, but higher figures were reported from isolated communities where patients did not have access to health centers, a situation similar to those reported from Africa in refugee settings under political instability. Although the epidemic spread to neighboring countries, it never reached the magnitude seen in Peru, which suffered that year from serious economic constraints and reported the lowest level of sanitary coverage and sanitary investment in the region. During 1991, approximately 50 percent of the population in urban cities of Peru received treated municipal water; intermittent supply and clandestine connections were common in many cities of the country (Figure 2-3). Additionally, less than 10 percent of sewerage water was treated properly. These conditions prevailed before the beginning of the epidemic and were responsible
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Global Issues in Water, Sanitation, and Health: Workshop Summary for its very rapid spread. The epidemic lasted for five years until 1995, only to reappear again in 1998 with much less intensity, as shown in Figure 2-4 (WHO, 2008). The message conveyed to the population at the beginning of the epidemic to curtail transmission focused on avoiding eating raw fish and shellfish and to boil water for drinking purposes. Massive investment in sanitation followed the epidemic, which was responsible for a reduction in transmission not only of cholera but also of other enteric infections, such as numerous parasitic infections and typhoid fever. The case of typhoid fever deserves special mention. Many experienced doctors in Lima saw a marked reduction in the incidence of typhoid fever in their practices as a consequence of improvements in sanitation and hygiene, a situation that was also seen at our Institute (Figure 2-5). FIGURE 2-3 A shantytown in Peru during 1991. SOURCE: Instituo de Medicina Tropical Alexander von Humboldt, Lima, Peru.
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Global Issues in Water, Sanitation, and Health: Workshop Summary FIGURE 2-4 Cholera in the Americas, 1991-2006. SOURCE: Based upon data compiled from and reported in the WHO’s Weekly Epidemiological Record. Before 1990, typhoid fever was responsible for the majority of episodes of undifferentiated fever lasting at least five days in Lima. Approximately 70 to 100 patients with complicated typhoid fever were hospitalized yearly in our institution the decade before the cholera epidemic; these figures were reduced tenfold after 1991. The reduction in typhoid fever incidence was so dramatic that the disease is almost unknown by the generation of physicians trained after 1991, with the subsequent delay in diagnosis and development of complications, an unthinkable situation the decade before 1990. Still, a question remains unanswered: From where did this huge cholera epidemic originate? Although both nontoxigenic O1 and non-O1 V. cholerae strains had been isolated from environmental sources and from patients in Peru and other countries in the region, the hypothesis that suggested that these Vibrio became residents in aquatic environments of coastal Peru with further acquisition of virulence genes that mediated for toxigenic expression through phage infection seems unlikely. Additionally, genetic comparison of the Vibrio responsible for the epidemic; V. cholerae O1 serotype Inaba and biotype El Tor, with endemic agents in Asia, disclosed very similar patterns, suggesting common ancestors or spread from one place to another. The latter option seems more reasonable. Another hypothesis suggests that V. cholerae was seeded into the marine ecosystems of northern Peru a few months before the epidemic started, which seems more likely in light of what was discussed earlier—that Vibrio was imported from Asia transported by crew ships, or emptied from vessels discharging bilge water contaminated with the bacterium. From its aquatic environment Vibrio was first amplified along the north coast
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Global Issues in Water, Sanitation, and Health: Workshop Summary FIGURE 2-5 Typhoid fever cases seen at the Alexander von Humboldt Tropical Medicine Institute in Lima, Peru, 1987-1993. and then introduced almost simultaneously into several cities of the country (Figure 2-6). This hypothesis was proposed after analyzing data generated by a retrospective study that reviewed charts of patients who had attended several hospitals along the Peruvian North Coast in 1989 and 1991, and disclosed that seven patients fulfilled the clinical definition of cholera proposed by the World Health Organization three months before the epidemic had started (Seas et al., 2000). These adult patients attended with severe dehydration and watery diarrhea, clinical presentation that had not been at these health centers the year before the epidemic. Although no convincing evidence proves definitively that these cases were due to cholera (clinical laboratory cultures had not been obtained for these cases), the clinical presentation is similar to that described in other epidemic areas for cholera, and also similar to that which many Peruvian doctors subsequently saw (Figure 2-7). Which Forces Drove the Spread of Vibrio into the Pacific Coastal Areas of Peru? Dr. Rita Colwell’s theory on the environmental niche for V. cholerae in aquatic ecosystems is crucial for understanding cholera dynamics. Factors that modify the survival of Vibrio in the environment may dramatically influence cholera transmission. Climate change and climate variability are among these
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Global Issues in Water, Sanitation, and Health: Workshop Summary FIGURE 2-6 The seventh cholera pandemic. SOURCE: Carlos Seas. Cólera. Medicina Tropical. CD-ROM. Version 2002. Instituto de Medicina Tropical, Príncipe Leopoldo. Amberes, Bélgica. Instituto de Medicina Tropical Alexander von Humboldt; Lima, Peru. Universidad Mayor de San Simón, Cochababmba, Bolivia.
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Global Issues in Water, Sanitation, and Health: Workshop Summary FIGURE 2-7 Location of patients in Peru with presumed cholera, identified before the epidemic of 1991. SOURCE: Reprinted from Seas et al. (2000) with permission from the American Journal of Tropical Medicine and Hygiene. critical forces. While the association between climate, environmental factors, and cholera transmission had been proposed a long time ago, the role of climate in cholera dynamics has been better elucidated in recent years. Time series analysis has demonstrated a relationship between the appearance of cholera cases in Bangladesh and occurrence of El Niño-Southern Oscillation (ENSO). Observations have linked the interannual variability of ENSO with the proportion of cholera cases in Dhaka, Bangladesh. Additionally, climate variability due to ENSO and temporary immunity explained the interannual cycles of cholera in rural Matlab, Bangladesh, for a period of almost 30 years (Pascual et al., 2000). The net effect of ENSO—rise in both sea water temperature and planktonic mass—modifies the abundance of V. cholerae in the environment by affecting the concentration of plankton to which V. cholerae is attached and affects the concentration of nutrients and salinity. Water temperature affects cholera transmission, as has been observed in the Bay of Bengal, Bangladesh. All these data support the role of ENSO in the interannual variability of endemic cholera. An unproven hypothesis suggests that El Niño triggered the epidemic of cholera in Peru in 1991 by amplifying the planktonic mass and dispersing existing Vibrio along the north coast of the
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Global Issues in Water, Sanitation, and Health: Workshop Summary country. Then Vibrio was introduced into the continent by contaminated food and subsequently by contamination of the water supply system (Seas et al., 2000). Several studies conducted in Peru after 1991 have shown an association between warmer air temperatures and cholera cases in children and adults. Additionally, toxigenic V. cholerae O1 has been isolated from aquatic environments in the coastal waters of Peru, suggesting that it has been successful in adapting to these environments, as has been described in Bangladesh and India. These findings support the theory of an environmental niche for V. cholerae O1 in Latin America and temporal associations between ENSO and cholera outbreaks from 1991 onward (Salazar-Lindo et al., 2008). The Spread of the Cholera Epidemic in Peru as a Model to Understand Transmission in the Region As illustrated earlier in Figure 2-3, the cholera transmission cycle involves infection of humans by the consumption of contaminated food and water and further shedding of the bacteria into the environment via contaminated stools. Incredibly high attack rates accompany human infection under favorable conditions, especially in previously nonexposed populations. Very high household transmission rates also occur. Transmission via contaminated water and food has been long recognized. During the Latin American epidemic, acquisition of the disease by drinking contaminated water from rivers, ponds, lakes, and even tube well sources were documented. Contamination of municipal water was the main route of cholera transmission in Trujillo, Peru, during the epidemic in 1991. Drinking unboiled water, introducing contaminated hands into containers used to store drinking water, drinking beverages from street vendors, drinking beverages when contaminated ice had been added, and drinking water outside the home are recognized exposure risk factors for cholera. In addition to the crucial role of water in the transmission of cholera, poor hygienic conditions also contribute to the spread of cholera by exposing susceptible persons to the pathogen. Educational campaigns were implemented throughout the country with little effect in the short term. Certain host factors may have played a role in the transmission of cholera. Infection by Helicobacter pylori, the effect of the O blood group, and the protective effect of breast milk deserve to be mentioned. Studies from Bangladesh and Peru show that people infected by H. pylori are at higher risk of acquiring cholera than people not infected by H. pylori (León-Barúa et al., 2006). Additionally, the risk of acquiring severe cholera among people coinfected with H. pylori is higher in patients without previous contact with V. cholerae, as measured by the absence of vibriocidal antibodies in the serum (Clemens et al., 1995). H. pylori is highly endemic in developing countries, particularly among low-income status individuals. Infection causes a chronic gastritis that induces hypochlorhydria, which in turn reduces the ability of the stomach to limit the
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Global Issues in Water, Sanitation, and Health: Workshop Summary samples from the farm near Well 5. Dr. A. Simor, the Inquiry’s expert on medical microbiology, described how pathogens were characterized in the laboratory (A. Simor, W. I. Transcript, February 26, 2000, pp. 142-146). Three methods were used to gain more evidence about the specific strains of pathogens identified: phage typing, serotyping and pulsed-field gel electrophoresis (PFGE). The first method exploits the ability of certain viruses to infect bacteria. These viruses are named bacteriophages—phages for short. Different bacteria are susceptible to infection by different phages, so exposing a strain of bacteria to a range of different phages can be used to type that strain for its susceptibility to phage attack. That pattern of phage susceptibility can be used to distinguish one strain of bacteria from another strain of the same species. The second method, serotyping, relies on detecting specific antigens on the exterior of a bacterial cell. These include O antigens that characterize components of the bacterial cell walls and H antigens that characterize the flagella (the whip-like tails that bacteria use for motion). For example, the name E. coli O157:H7 refers to the strain of E. coli with the 157 antigen in the cell wall and the 7 antigen in the flagellum. Individual strains of Campylobacter species, such as C. jejuni, can also be characterized by serotyping. The third method, PFGE, looks at the molecular properties of the DNA found in a bacterial strain. Because the DNA provides the genetic material that causes specific strains of a bacterial species to be distinct, evaluating and comparing the DNA of individual strains provides a relatively direct method for identifying specific strains. In this procedure, DNA is extracted from the bacterial cell and is cut at chosen locations using specific enzymes to yield DNA fragments of varying size. These fragments are separated on a gel plate by electrophoresis to yield a pattern of bands distributed according to the relative size of the fragments. The resulting pattern can be interpreted in terms of the original DNA structure to compare with DNA from different strains. Identical strains will have identical DNA fragment patterns, while the patterns of closely related strains may differ in only a few fragments. Dr. Simor’s expert opinion at the Inquiry (A. Simor, W. I. Transcript, p. 160, February 26) was that strains differing by six or fewer DNA fragment bands are considered genetically related in the context of a common source for an outbreak. These advanced methods were used to compare pathogens recovered from cattle manure with those from infected humans. By August 31, 2000, in the follow-up investigation, the outbreak team working for the Health Unit had identified 1,730 cases as suspected cases (BGOSHU, 2000). Following contact attempts by phone or mail, 80 percent of contacts were judged to have an illness related to exposure to Walkerton municipal water, and 1,346 cases met the definition adopted for the investigation. “A case was defined as a person with diarrhea, or bloody diarrhea; or stool specimens presumptive positive for E. coli O157 or Campylobacter spp. or HUS between April 15 to June 30. For the purposes of attributing cases to the water system, a primary
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Global Issues in Water, Sanitation, and Health: Workshop Summary case was defined as a person who had exposure to Walkerton water. A secondary case was defined as a person who did not have any exposure to Walkerton water but had exposure to a primary case as defined above. A person was classified as unknown if their exposure status was not indicated” (BGOSHU, 2000). Of these cases, 675 had submitted stool samples for culture, yielding 163 positive for E. coli O157:H7, 97 positive for C. jejuni, 7 positive for C. coli and 12 positive for both E. coli O157:H7 and Campylobacter. The outbreak curve is plotted in Figure 2-18. The second peak in the epidemic curve (Figure 2-18) has been discussed as possibly representing the second of two types of infection that occurred, with C. jejuni and with E. coli. Another possibility that was not discussed is that the second peak occured on May 23, the date that Dr. McQuigge gave his first press conference on the outbreak. The resulting high profile media coverage that day might have anchored May 23 in the memories of some victims when they responded to the survey performed later to determine the date of onset of illness for each case. Various cultures were also done on environmental samples, allowing some comparison with the pathogens causing illness. The Health Unit collected samples from 21 sites in the Walkerton distribution system on May 21 and collected raw and treated water from Well 5 on May 23. Concurrent samples taken at Wells 6 and 7 showed neither total coliforms nor E. coli. Two of the distribution system sites remained positive for total coliforms and E. coli over several days. One of the distribution system sites, along with cultures from the May 23 raw and treated water samples from Well 5, was analyzed by PCR, another molecular diagnostic technique. This technique is able to amplify DNA from a sample to allow extremely sensitive detection for specific genes that may be present. Using PCR, these samples, representing a contaminated location in the Walkerton distribution system and Well 5, all showed the same genes for O157, H7 and the specific verotoxin, VT2. Working with Health Canada and the Ontario Ministry of Agriculture and Food, the Health Unit undertook livestock sampling on farms within a 4 km radius of each of Wells 5, 6, and 7 between May 30 and June 13 (BGOSHU, 2000). They obtained livestock fecal samples from 13 farms and found human pathogens (mainly Campylobacter) in samples from 11. On two farms, both C. jejuni and E. coli O157:H7 were found. These farms were selected for further sampling on June 13. The results are summarized in Table 2-1. Farm 1 was located in the vicinity of Wells 6 and 7 and Farm 2 was located within sight of Well 5 (Figure 2-17). The most telling features of these typing efforts are revealed in Table 2-2, which compares the strain characteristics from the cattle fecal samples at the two farms with the cultures from human cases infected with E. coli O157:H7 or Campylobacter spp. Details of the extensive strain typing work that was done have now been published by Clark et al. (2003).
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Global Issues in Water, Sanitation, and Health: Workshop Summary TABLE 2-1 Culture Results from Two Farms Resampled on June 13 Pathogens Number Positive Farm 1 Farm 2 E. coli O157:H7 2 6 C. jejuni/coli 8 9 Both 2 — SOURCE: Derived from data reported in BGOSHU (2000) and reprinted from Hrudey and Hrudey (2004) with permission from IWA Publishing. TABLE 2-2 Pathogen Strain Typing Comparison Between Human Cases and Cattle Fecal Samples at Farms 1 and 2 Human Cases Cattle Fecal Samples Farm 1 Farm 2 Total individuals tested 675 20 38 E. coli O157:H7 positive 163 4 6 Phage type 14 147 (90% of +) 0 6 (100% of +) Phage type 14a 3 (2% of +) 4 (100% of +) 0 PFGE pattern A 150 (92% of +) 0 6 (100% of +) PFGE pattern A1 2 (1.2% of +) 4 (100% of +) 0 PFGE pattern A4 2 (1.2% of +) 0 1 (17% of +) Verotoxin VT2 majority – 6 (100% of +) Campylobacter spp. positive 105 8 9 Phage type 33 56 (53% of +) 0 9 (100% of +) Other phage types 2, 13, 19var, 44, 77 8 (100% of +) 0 SOURCE: Derived from data reported in BGOSHU (2000) and reprinted from Hrudey and Hrudey (2004) with permission from IWA Publishing. These results do not provide absolute confirmation that manure from Farm 2 was responsible for contamination of the Walkerton water supply for a number of reasons. The cattle samples were taken in mid-June, about a month after the suspected date of contamination, and it is not possible to be certain that cattle on Farm 2 were infected on May 12. Likewise, the DNA typing by PFGE must be recognized as much less certain than DNA typing used in human forensic analysis. Because bacteria reproduce by binary fission, each progeny cell is a clone of its parent (i.e., each progeny cell
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Global Issues in Water, Sanitation, and Health: Workshop Summary has identical DNA to the parent cell, so individual cells are not genetically unique). However, the DNA makeup of bacteria changes rapidly because their rapid rate of reproduction allows genetic mutation through a number of mechanisms that alters their DNA quickly compared with humans. In total, the level of evidence for this outbreak is far more compelling than the quality and level of evidence that has historically been available for outbreak investigations. The main features suggesting that Farm 2, located near Well 5, was the primary source of pathogens that caused the outbreak are the match of the phage type 14 for E. coli O157:H7, with PFGE pattern A and with phage type 33 for the Campylobacter spp. Finding that raw water in Well 5 was contaminated by pathogens detected in cattle manure from a nearby farm does not explain how this contamination was allowed to cause the disastrous disease outbreak in the community. The water produced by all the wells serving Walkerton was supposed to be chlorinated continuously to achieve a chlorine residual of 0.5 mg/L for 15 minutes of contact time (ODWO). This level of disinfection would have provided a concentration-contact time (CT) value of 7.5 mg/L-min. That CT value is more than 150 times greater than literature CT values of 0.03-0.05 mg-min/L for 99 percent inactivation of E. coli O157:H7 and more than 80 times greater than a CT value of 0.067 to 0.090 mg-min/L for 99.99% inactivation of E. coli (Hoff and Akin, 1986; Kaneko, 1998). Clearly, the specified level of chlorine residual and contact time was not operative for Well 5 in May 2000. If it had been, inactivation of the E. coli pathogen greater than 99.99 percent would have been achieved, a level of protection that is certainly not consistent with the magnitude of the outbreak that occurred in Walkerton.16 Indirect Causes of the Walkerton Outbreak Although the PUC operators were obviously culpable for their misdeeds of omission and commission, they were clearly not the sole cause of this disaster. The overwhelming impression that follows from reviewing what happened in Walkerton is that complacency was pervasive at many levels. The majority of the discussion of the cause of this disaster in the Part 1 Walkerton Inquiry report (O’Connor, 2002a) was devoted to evaluating the contributions from many other parties to this disaster. Those interested in pursuing the institutional failures are referred to the Inquiry report. A brief summary of those institutional failures is provided below. The Ontario Ministry of Environment The original certificate of approval was issued in 1978 for Well 5 without including any formal operating conditions to deal with the hazards that were apparent from the pump testing at the commissioning of this well. 16 End Hrudey and Hrudey (2004) text.
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Global Issues in Water, Sanitation, and Health: Workshop Summary In 1994 the MOE adopted a policy to require continuous chlorine residual monitoring for vulnerable shallow wells (under the influence of surface contamination) but the MOE failed to implement policy this for existing vulnerable wells like Well 5. There was no follow-up on deficiencies identified during rare inspections including one that was conducted in 1998 which identified some of the deficiencies in the monitoring practices of the PUC operators. The false records and clear deficiencies in performance of the Walkerton operators were not recognized by the MOE. The MOE showed surprisingly little institutional knowledge about drinking water safety. The Walkerton Public Utilities Commission The PUC placed total confidence in their General Manager and it took no apparent interest or responsibility for oversight of PUC operations. The PUC ignored an adverse MOE inspection report in 1998 and demonstrated no interest in assuring that the PUC was responding to the deficiencies identified. The PUC maintained a substantial financial surplus while not making investments in improving the water system. The PUC took an adversarial stance with the Health Unit when the outbreak occurred. The Government of Ontario The Ontario government slashed the budget of the MOE drastically (>40 percent) over the previous five years with little evidence of concern for consequences to public health. Responsibility for drinking water safety was largely offloaded to individual communities without providing effective assistance for these communities to handle that responsibility. Water testing was removed from the provincial laboratory without adding any regulatory requirement for mandatory reporting of adverse results by the private labs to the MOE or the local health units. Preventing Drinking Water Outbreaks: Turning Hindsight into Foresight The challenge in preventing drinking water disasters like Walkerton is to learn from the experience of such disasters. There have been a surprising number of drinking water outbreaks in affluent countries and many have features in common with Walkerton (Hrudey and Hrudey, 2004). The task is essentially one of
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Global Issues in Water, Sanitation, and Health: Workshop Summary turning hindsight into foresight. This requires a risk management approach that demands a committed focus on prevention, as evidenced by: Informed vigilance, is actively promoted and rewarded. Understanding of the entire water system, from source to consumer’s tap, its challenges and limitations, is promoted and actively maintained. Effective, real-time treatment process control is the basic operating approach. Fail-safe multi-barriers are actively identified and maintained at a level appropriate to the challenges facing the system. Close calls are documented and used to train staff about how the system responded under stress and to identify what measures are needed in future. Operators, supervisors, lab personnel and management all understand that they are entrusted with protecting the public’s health and are committed to honoring that responsibility above all else. Operational personnel are afforded the status, training, and remuneration commensurate with their responsibilities as guardians of the public’s health. Response capability and communication are enhanced. An overall continuous improvement, total quality management mentality will pervade the organization (Hrudey and Hrudey, 2004). Justice O’Connor concluded in his second Inquiry report (O’Connor, 2002b) that “Ultimately, the safety of drinking water is protected by effective management systems and operating practices, run by skilled and well-trained staff.” Ontario has committed to implementing substantial improvements in the scope and quality of operator training. Operators can prevent a disaster like Walkerton if they assure the following key elements are established and followed (Hrudey and Walker, 2005): Operators must understand their system, including the major contamination hazards it faces in relation to the safety barriers and their capabilities for assuring safe water. Operators must develop guidance limits for monitoring parameters that are able to detect abnormal conditions, based on knowing their system. Operators must watch for and recognize signals for abnormal conditions (i.e., increase in turbidity or chlorine demand and drop of chlorine residual). Operators must work with management to anticipate plausible abnormal conditions and plan effective responses well before a serious incident occurs, including appropriate notification of regulatory authorities. Pre-
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Global Issues in Water, Sanitation, and Health: Workshop Summary paredness should support but does not replace the need for thoughtful analysis and problem-solving as events unfold. Operators must recognize when they are facing a problem that is beyond their understanding or training and call for assistance. Operators’ understanding of their system should include recognition of any inherent vulnerability that needs improvement to reduce contamination risks. Operators need to be prepared to take ownership of problems and lead efforts to ensure that their managers fully understand the existence of such problems that must be rectified. Concluding Comments The Walkerton outbreak provides a strong argument for the multiple barrier approach for assuring safe drinking water. This needs to be based on a preventive risk management approach like that described in the Australian Drinking Water Guidelines (NHMRC, 2004) or the WHO water safety plan approach (WHO, 2004) that is firmly grounded in a quality management approach that is founded on a thorough understanding of the risks facing any particular system (Hrudey, 2004). Because outbreaks of disease caused by drinking water remain comparatively rare in North America, particularly in contrast with the developing world, complacency about the dangers of waterborne pathogens can easily occur. Yet, the source of waterborne disease in the form of microbial pathogens is an ever present risk because these pathogens are found in human fecal waste and in fecal wastes from livestock, pets or wildlife, making any drinking water source at risk of contamination before or after treatment (Hrudey, 2006b). SEAS AND GOTUZZO REFERENCES Clemens, J., M. J. Albert, M. Rao, F. Qadri, S. Huda, B. Kay, F. P. van Loon, D. Sack, B. A. Pradhan, and R. B. Sack. 1995. Impact of infection by Helicobacter pylori on the risk and severity of endemic cholera. Journal of Infectious Diseases 171(6):1653-1656. Colwell, R. R., M. L. Tamplin, P. R. Brayton, A. L. Gauzens, B. D. Tall, D. Herrington, M. M. Levine, S. Hall, A. Huq, and D. A. Sack. 1990. Environmental aspects of Vibrio cholerae in transmission of cholera. In Advances in Research on Cholera and Related Diarrheas, vol. 7, edited by R. B. Sack, and Y Zinnaka. Tokyo: KTK Scientific. Colwell, R. R., A. Huq, M. S. Islam, K. M. A. Aziz, M. Yunus, N. Huda Khan, A. Mahmud, R. Bradley Sack, G. B. Nair, J. Chakraborty, D. A. Sack, and E. Russek-Cohen. 2003. Reduction of cholera in Bangladeshi villages by simple filtration. Proceedings of the National Academy of Sciences 100(3):1051-1055. Franco, A. A., A. D. Fix, A. Prada, E. Paredes, J. C. Palomino, A. C. Wright, J. A. Johnson, R. McCarter, H. Guerra, and J. G. Morris, Jr. 1997. Cholera in Lima, Peru, correlates with prior isolation of Vibrio cholerae from the environment. American Journal of Epidemiology 146(12):1067-1075.
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Global Issues in Water, Sanitation, and Health: Workshop Summary Gotuzzo, E., J. Cieza, L. Estremadoyro, and C. Seas. 1994. Cholera: lessons from the epidemic in Peru. Infectious Disease Clinics of North America 8(1):183-205. León-Barúa, R., S. Recavarren-Arce, E. Chinga-Alayo, C. Rodríguez-Ulloa, D. N. Taylor, E. Gotuzzo, M. Kosek, D. Eza, and R. H. Gilman. 2006. Helicobacter pylori-associated chronic atrophic gastritis involving the gastric body and severe disease by Vibrio cholerae. Transactions of the Royal Society of Tropical Medicine and Hygiene 100(6):567-572. Lipp, E. K., A. Huq, and R. R. Colwell. 2002. Effects of global climate on infectious disease: the cholera model. Clinical Microbiology Reviews 15(4):757-770. Pascual, M., X. Rodó, S. P. Ellner, R. Colwell, and M. J. Bouma. 2000. Cholera dynamics and El Niño-southern oscillation. Science 289(5485):1766-1769. Salazar-Lindo, E., C. Seas, and D. Gutierrez. 2008. The ENSO and cholera in South America: what we can learn about it from the 1991 cholera outbreak. International Journal of Environment and Health 2(1):30-36. Seas, C., J. Miranda, A. I. Gil, R. Leon-Barua, J. Patz, A. Huq, R. R. Colwell, and R. B. Sack. 2000. New insights on the emergence of cholera in Latin America during 1991: the Peruvian experience. American Journal of Tropical Medicine and Hygiene 62(4):513-517. WHO (World Health Organization). 2008. Cholera. Weekly Epidemiological Record 83(31):269-284. Zuckerman, J. N., L. Rombo, and A. Fisch. 2007. The true burden and risk of cholera: implications for prevention and control. Lancet Infectious Diseases 7(8):521-530. DAVIS REFERENCES Addiss, D. G., W. R. Mac Kenzie, N. J. Hoxie, M. S. Gradus, K. A. Blair, M. E. Proctor, J. J. Kazmierczak, W. L. Schell, P. Osewe, H. Frisby, H. Cicirello, R. L. Cordell, J. B. Rose, and J. P. Davis. 1995. Epidemiologic features and implications of the Milwaukee cryptosporidiosis outbreak. In Protozoan parasites and water, edited by W. B. Betts, D. Casemore, C. Fricker, H. Smith, and J. Watkins. Cambridge, UK: The Royal Society of Chemistry. Pp. 19-25. Addiss, D. G., R. S. Pond, M. Remshak, D. Juranek, S. Stokes, and J. P. Davis. 1996. Reduction of risk of watery diarrhea with point-of-use water filters during a massive outbreak of waterborne Cryptosporidium infection in Milwaukee, 1993. American Journal of Tropical Medicine and Hygiene 54(6):549-553. CDC (Centers for Disease Control and Prevention). 1994. Cryptosporidium infections associated with swimming pools—Dane County, Wisconsin, 1993. Morbidity and Mortality Weekly Report 43(31):561-563. Chappell, C. L., P. C. Okhuysen, R. C. Langer-Curry, G. Widmer, D. E. Akiyoshi, S. Tanriverdi, and S. Tzipori. 2006. Cryptosporidium hominis: experimental challenge of healthy adults. American Journal of Tropical Medicine and Hygiene 75(5):851-857. Cicirello, H. G., K. S. Kehl, D. G. Addiss, M. J. Chusid, R. I. Glass, J. P. Davis, and P. L. Havens. 1997. Cryptosporidiosis in children during a massive waterborne outbreak, Milwaukee, Wisconsin: clinical, laboratory, and epidemiologic findings. Epidemiology and Infection 119(1):53-60. Cordell, R. L., D. G. Addiss, P. Thor, J. Theurer, R. Lichterman, S. Ziliak, F. Steurer, D. D. Juranek, and J. P. Davis. 1997. Impact of a massive waterborne cryptosporidiosis outbreak on child care facilities in metropolitan Milwaukee, Wisconsin. Pediatric Infectious Diseases Journal 16(7):639-644. Corso, P. S., M. H. Kramer, K. A. Blair, D. G. Addiss, J. P. Davis, A. C. Haddix. 2003. The cost of illness in the waterborne Cryptosporidium outbreak, Milwaukee, Wisconsin. Emerging Infectious Diseases 9(4):426-431. Current, W. L., N. C. Reese, J. V. Ernst, W. S. Bailey, M. B. Heyman, and W. M. Weinstein. 1983. Human cryptosporidiosis in immunocompetent and immunodeficient persons: studies of an outbreak and experimental transmission. New England Journal of Medicine 308(21):1252-1257.
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Global Issues in Water, Sanitation, and Health: Workshop Summary D’Antonio, R. G., R. E. Winn, J. P. Taylor, T. L. Gustafson, W. L. Current, M. M. Rhodes, G. W. Gary, Jr., and R. A. Zajac. 1985. A waterborne outbreak of cryptosporidiosis in normal hosts. Annals of Internal Medicine 103(6 Pt 1):886-888. Du Pont, H. L., C. L. Chappell, C. R. Sterling, P. C. Okhuysen, J. B. Rose, and W. Jakubowski. 1995. The infectivity of Cryptosporidium parvum in health volunteers. New England Journal of Medicine 332(13):855-859. Fayer, R. 2004. Cryptosporidium: a water-borne zoonotic parasite. Veterinary Parasitology 126(1-2):37-56. Frisby, H. R., D. G. Addiss, W. J. Reiser, B. Hancock, J. M. Vergeront, N. J. Hoxie, and J. P. Davis. 1997. Clinical and epidemiologic features of a massive waterborne outbreak of cryptosporidiosis among persons with human immunodeficiency virus (HIV) infection. Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology 16(5):367-373. Gallagher, M. M., J. L. Herndon, I. J. Nims, C. R. Sterling, D. J. Grabowski, and H. F. Hull. 1989. Cryptosporidiosis and surface water. American Journal of Public Health 79(1):39-42. Hayes, E. B., T. D. Matte, T. R. O’Brien, T. W. McKinley, G. S. Logsdon, J. B. Rose, B. L. Ungar, D. M. Word, P. F. Pinsky, M. L. Cummings, M. A. Wilson, E. G. Long, E. S. Hurwitz, and D. D. Juranek. 1989. Large community outbreak of cryptosporidiosis due to contamination of a filtered public water supply. New England Journal of Medicine 320(21):1372-1376. Hoxie, N. J., J. P. Davis, J. M. Vergeront, R. D. Nashold, and K. A. Blair. 1997. Cryptosporidiosis-associated mortality following a massive waterborne outbreak in Milwaukee, Wisconsin. American Journal of Public Health 87(12):2032-2035. Joseph, C., G. Hamilton, M. O’Connor, S. Nicholas, R. Marshall, R. Stanwell-Smith, R. Sims, E. Ndawula, D. Casemore, P. Gallagher, and P. Harnett. 1991. Cryptosporidiosis in the Isle of Thanet: an outbreak associated with local drinking water. Epidemiology and Infection 107(3):509-519. Juranek, D. D., D. G. Addiss, M. E. Bartlett, M. J. Arrowood, D. G. Colley, J. E. Kaplan, R. Perciasepe, J. R. Elder, S. E. Regli, and P. S. Berger. 1995. Cryptosporidiosis and public health: workshop report. Journal of the American Water Works Association 87(9):69-80. Leland, D., J. McAnulty, W. Keene, and G. Stevens. 1993. A cryptosporidiosis outbreak in a filtered-water supply. Journal of the American Water Works Association 85(6):34-42. Mac Kenzie, W. R., D. G. Addiss, and J. P. Davis. 1994a. Cryptosporidium and the public water supply. New England Journal of Medicine 331(22):1529-1530. Mac Kenzie, W. R., N. J. Hoxie, M. E. Proctor, M. S. Gradus, K. A. Blair, D. E. Peterson, J. J. Kazmierczak, D. G. Addiss, K. R. Fox, J. B. Rose, and J. P. Davis. 1994b. A massive outbreak in Milwaukee of Cryptosporidium infection transmitted through the public water supply. New England Journal of Medicine 331(3):161-167. Mac Kenzie, W. R., J. J. Kazmierczak, and J. P. Davis. 1995a. Cryptosporidiosis associated with a resort swimming pool. Epidemiology and Infection 115(3):545-553. Mac Kenzie, W. R., W. L. Schell, K. A. Blair, D. G. Addiss, D. E. Peterson, N. J. Hoxie, J. J. Kazmierczak, and J. P. Davis. 1995b. Massive outbreak of waterborne Cryptosporidium infection in Milwaukee, Wisconsin: recurrence of illness and risk of secondary transmission. Clinical Infectious Diseases 21(1):57-62. McDonald, A. C., W. R. Mac Kenzie, D. G. Addiss, M. S. Gradus, G. Linke, E. Zembrowski, M. R. Hurd, M. J. Arrowood, P. J. Lammie, and J. W. Priest. 2001. Cryptosporidium parvum–specific antibody responses among children residing in Milwaukee during the 1993 waterborne outbreak. Journal of Infectious Diseases 183(9):1373-1379. Meisel, J. L., D. R. Perera, C. Meligro, and C. E. Rubin. 1976. Overwhelming watery diarrhea associated with Cryptosporidium in an immunosuppressed patient. Gastroenterology 70(6):1156-1160. Morgan-Ryan, U. M., A. Fall, L. A. Ward, N. Hijawi, I. Sulaiman, R. Payer, R. C. Thompson, M. Olson, A. Lal, and L. Xiao. 2002. Cryptosporidium hominis n. sp. (Apicomplexa: Cryptosporidiidae) from Homo sapiens. Journal of Eukaryotic Microbiology 49(6):433-440.
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