Guidance on Waterborne Bacterial Pathogens

Guidance on Waterborne Bacterial Pathogens
Guidance on
Waterborne Bacterial
Pathogens
Health Canada is the federal department responsible for helping the people of Canada
maintain and improve their health. We assess the safety of drugs and many consumer
products, help improve the safety of food, and provide information to Canadians to help
them make healthy decisions. We provide health services to First Nations people and to
Inuit communities. We work with the provinces to ensure our health care system serves the
needs of Canadians.
Published by authority of the Minister of Health.
Guidance on waterborne bacterial pathogens
is available on Internet at the following address:
www.healthcanada.gc.ca
Également disponible en français sous le titre :
Conseils sur les bactéries pathogènes d’origine hydrique
This publication can be made available on request in a variety of alternative formats.
© Her Majesty the Queen in Right of Canada,
represented by the Minister of Health, 2013
This publication may be reproduced without permission provided the source is fully
acknowledged.
Pub. Number: 130469
Cat.: H129-25/1-2014E-PDF
ISBN: 978-1-100-22966-9
Guidance on
Waterborne Bacterial
Pathogens
Prepared by the
Federal-Provincial-Territorial Committee on
Drinking Water
of the
Federal-Provincial-Territorial Committee on
Health and the Environment
Health Canada
Ottawa, Ontario
February 2013
FPT Committee on Drinking Water
February 2013
This document may be cited as follows:
Health Canada (2013). Guidance on waterborne bacterial pathogens. Water, Air and Climate
Change Bureau, Healthy Environments and Consumer Safety Branch, Health Canada, Ottawa,
Ontario (Catalogue No. H129-25/1-2014E-PDF).
The document was prepared by the Federal-Provincial-Territorial Committee on Drinking Water
of the Federal-Provincial-Territorial Committee on Health and the Environment.
Any questions or comments on this document may be directed to:
Water and Air Quality Bureau
Healthy Environments and Consumer Safety Branch
Health Canada
269 Laurier Avenue West, Address Locator 4903D
Ottawa, Ontario
Canada K1A 0K9
Tel.: 613-948-2566
Fax: 613-952-2574
E-mail: [email protected]
Other documents concerning Canadian drinking water quality can be found on the following
website: www.healthcanada.gc.ca/waterquality
Table of Contents
Background on guidance documents ............................................................................................ 1
Part A. Guidance on waterborne bacterial pathogens................................................................ 2
Part B. Supporting information .................................................................................................... 4
B.1
Waterborne faecal pathogens ............................................................................................ 4
B.1.1 Pathogenic Escherichia coli ..................................................................................... 4
B.1.1.1 Treatment technology ............................................................................... 5
B.1.1.2 Assessment ................................................................................................ 6
B.1.2 Salmonella and Shigella ........................................................................................... 6
B.1.2.1 Treatment technology ............................................................................... 7
B.1.2.2 Assessment ................................................................................................ 7
B.1.3 Campylobacter and Yersinia .................................................................................... 7
B.1.3.1 Treatment technology ............................................................................... 8
B.1.3.2 Assessment ................................................................................................ 8
B.2
Waterborne non-faecal pathogens .................................................................................... 8
B.2.1 Legionella ................................................................................................................. 9
B.2.1.1 Sources and exposure ................................................................................ 9
B.2.1.2 Health effects .......................................................................................... 11
B.2.1.3 Treatment technology ............................................................................. 11
B.2.1.4 Assessment .............................................................................................. 13
B.2.2 Mycobacterium avium complex ............................................................................. 14
B.2.2.1 Sources and exposure .............................................................................. 14
B.2.2.2 Health effects .......................................................................................... 16
B.2.2.3 Treatment technology ............................................................................. 16
B.2.2.4 Assessment .............................................................................................. 18
B.2.3 Aeromonas .............................................................................................................. 18
B.2.3.1 Sources and exposure .............................................................................. 19
B.2.3.2 Health effects .......................................................................................... 21
B.2.3.3 Treatment technology ............................................................................. 22
B.2.3.4 Assessment .............................................................................................. 23
B.2.4 Helicobacter pylori ................................................................................................ 24
B.2.4.1 Sources and exposure .............................................................................. 24
B.2.4.2 Health effects .......................................................................................... 25
B.2.4.3 Treatment technology ............................................................................. 26
B.2.4.4 Assessment .............................................................................................. 27
B.3
Issues of emerging interest .............................................................................................. 27
B.3.1 Disinfection and antibiotic-resistant organisms ..................................................... 27
B.3.2 Showerheads........................................................................................................... 28
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February 2013
Residential-scale treatment ............................................................................................. 28
B.4.1 Residential-scale and private drinking water systems............................................ 28
B.4.2 Use of residential-scale treatment devices ............................................................. 29
Part C. References and acronyms ............................................................................................... 31
C.1
References ......................................................................................................................... 31
C.2
List of acronyms ............................................................................................................... 55
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Guidance on waterborne bacterial pathogens
Background on guidance documents
The main role of the Federal-Provincial-Territorial Committee on Drinking Water is the
development of the Guidelines for Canadian Drinking Water Quality. This role has evolved over
the years, and new methodologies and approaches have led the Committee to develop a new type
of document, guidance documents, to provide advice and guidance on issues related to drinking
water quality for parameters that do not require a formal guideline under the Guidelines for
Canadian Drinking Water Quality.
There are two instances in which the Federal-Provincial-Territorial Committee on
Drinking Water may choose to develop a guidance document. The first would be to provide
operational or management guidance related to specific drinking water–related issues (e.g., boil
water advisories), in which case the document would provide only limited scientific information
or health risk assessment. The second instance would be to make health risk assessment
information available when a guideline is not deemed necessary.
The Federal-Provincial-Territorial Committee on Drinking Water establishes guidelines
under the Guidelines for Canadian Drinking Water Quality specifically for contaminants that
meet all of the following criteria:
1. exposure to the contaminant could lead to adverse health effects;
2. the contaminant is frequently detected, or could be expected to be found, in a large
number of drinking water supplies throughout Canada; and
3. the contaminant is detected, or could be expected to be detected, at a level that is of
possible health significance.
If a contaminant of interest does not meet all these criteria, the Federal-Provincial-Territorial
Committee on Drinking Water may choose not to establish a numerical guideline or develop a
guideline technical document. In such a case, a guidance document may be developed.
Guidance documents undergo a similar process as guideline technical documents,
including public consultations through the Health Canada website. They are offered as
information for drinking water authorities and, in some cases, to provide guidance in spill or
other emergency situations.
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Part A. Guidance on waterborne bacterial pathogens
This document provides information as background for those interested in drinking water
quality and safety. There is a particular focus on waterborne bacterial pathogens that may not
have the classical faecal–oral transmission route, as these may be less well known to the water
industry and public health professionals. Although there is information available from many
countries, this document emphasizes studies most relevant to the North American situation.
Throughout history, consumption of drinking water supplies of poor sanitary quality has
been linked to illnesses in human populations. These illnesses most commonly present as
gastrointestinal-related symptoms, such as diarrhoea and nausea. The organisms identified within
this document as waterborne faecal bacterial pathogens are those that have been well established
as having a history of being responsible for waterborne outbreaks of gastrointestinal illness.
There are standardized methods available for detecting and measuring certain pathogenic
bacteria in drinking water. However, routine monitoring for these organisms still remains
difficult and impractical. This is because there are a number of types of bacterial pathogens that
can be present in human and/or animal wastes, which can vary significantly in their distribution,
depending on the sources of contamination affecting the water supply; and because conducting
detection and identification procedures for each possible type can be difficult, requiring
significant resources. As a result, monitoring for a broad indicator of faecal contamination such
as Escherichia coli is useful in verifying the microbiological quality and safety of the drinking
water supply. The presence of E. coli in drinking water system indicates that the source or the
system has likely been affected by recent faecal contamination; as a result, the water should be
deemed as unsafe to drink.
In recent decades, there has been an increasing amount of interest in waterborne bacterial
pathogens that occur naturally in the water environment and thus have the potential to be
transmitted through water. The waterborne non-faecal bacterial pathogens discussed within this
document can cause human infection, resulting in gastrointestinal and non-gastrointestinal
illnesses (particularly respiratory illnesses). Routine monitoring for these pathogens remains
difficult and expensive as well. As these organisms occupy different environmental niches and
have primary sources other than human or animal faeces, there are at present no satisfactory
microbiological indicators for their presence. To date, none of these organisms has been
associated with outbreaks of illness as a result of ingestion of drinking water in Canada.
However, as they do have the potential to be spread through drinking water, it is important to
ensure that the treatment and disinfection strategies in place are capable of providing adequate
control of these organisms. Health Canada maintains that the best means of safeguarding against
the presence of waterborne pathogens (including non-faecal bacterial pathogens) in drinking
water is the application of the multibarrier approach, which includes adequate treatment, a wellmaintained distribution system and, in the case of enteric bacteria, source protection. Treatment
and disinfection requirements in the provision of microbiologically safe drinking water are based
on health-based treatment goals for the removal and inactivation of the enteric protozoa Giardia
and Cryptosporidium and enteric viruses. These organisms present a significant challenge to
water treatment and disinfection technologies because of their difficulty of removal, high
infectivity and high disinfectant resistance. As a result, current drinking water treatment and
disinfection practices applied to meet the treatment goals for viruses and protozoa are expected to
be similarly capable of controlling waterborne bacterial pathogens in drinking water. This
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approach can reduce both faecal and non-faecal pathogens to non-detectable levels or to levels
that have not been associated with human illness.
Consequently, it remains unnecessary and impractical to establish maximum acceptable
concentrations for the waterborne bacterial pathogens described in this document. The
monitoring of E. coli continues to be used in the verification of the microbiological quality of
drinking water. Information on the adequacy of drinking water treatment and on the microbial
condition of the distribution system is provided by the monitoring of E. coli and other indicators,
such as disinfectant residual and turbidity.
Under the multibarrier approach to safe drinking water, numerous process controls are
required to function alongside bacteriological analysis in order to reliably produce drinking water
of an acceptable quality. Important individual elements under this approach include:
source water protection (where possible);
optimized treatment performance (e.g., for turbidity reduction and particle removal);
proper application of disinfection technologies;
a well-designed and well-maintained distribution system; and
maintenance of a disinfectant residual.
The potential for the introduction of waterborne bacterial pathogens into the distribution
system and their ability to survive and regrow in biofilms are of concern in drinking water
treatment. Recurring patterns of elevated heterotrophic plate counts downstream of water
treatment may indicate the presence of biofilms, which could be a source of waterborne
pathogens. As microorganisms in biofilms may survive, multiply and be released into the
distribution system, water that meets the bacteriological guidelines may be recontaminated over
time.
Additional considerations specific for aiding in the control of biofilms in the distribution
system can include:
use of proper construction materials;
control measures to reduce levels of natural organic matter, scaling and corrosion;
measures to prevent low flow rates or water stagnation and to control temperatures (where
possible);
maintenance activities, such as flushing and cleaning; and
ensuring adequate disinfection after installation of new pipes and after maintenance or repair
of existing pipes.
Contamination problems involving waterborne bacterial pathogens can occur in water
systems beyond the water treatment plants’ distribution network, such as plumbing systems or
heating, ventilation and air conditioning systems. Specific information pertaining to guidance and
requirements for these systems can be found by consulting the proper regulatory authority.
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Part B. Supporting information
B.1
Waterborne faecal pathogens
Waterborne faecal pathogens are microorganisms that can occur in water as a result of
contamination from human or animal faeces and cause gastrointestinal illness. They are often
associated with bacteria from the Enterobacteriaceae family. Faecal bacteria that are well
established as having a history of being responsible for waterborne outbreaks of gastrointestinal
illness include pathogenic Escherichia coli, Salmonella, Shigella, Campylobacter and Yersinia.
B.1.1 Pathogenic Escherichia coli
Escherichia coli are bacteria found naturally in the digestive tracts of warm-blooded
animals, including humans. As such, E. coli are used in the drinking water industry as the
definitive indicator of recent faecal contamination of water. Escherichia coli are Gram-negative,
facultative anaerobic, rod-shaped bacteria, approximately 0.5–2 µm in size (AWWA, 2006).
Whereas most strains of E. coli are non-pathogenic, some possess virulence traits that enable
them to cause serious diarrhoeal infections in humans. These pathogenic E. coli are divided into
groups based on the mechanisms with which they interact with the human intestinal tract and
cause symptoms (e.g., some produce specific types of toxin, whereas others invade, bind to or
cause structural alterations of intestinal cells) (Percival et al., 2004). The six groups are
enterohaemorrhagic (EHEC), enterotoxigenic (ETEC), enteroinvasive (EIEC), enteropathogenic
(EPEC), enteroaggregative (EAEC) and diffuse adherent (DAEC) E. coli (Percival et al., 2004;
AWWA, 2006). The EHEC group has emerged as a group that is of particular significance to the
water industry (AWWA, 2006). This broad group contains many different serotypes that have
been implicated as causes of human illness (Muniesa et al., 2006).
One member of the EHEC group, E. coli O157:H7, has been most commonly associated
with pathogenic E. coli outbreaks worldwide (Muniesa et al., 2006) and has been implicated in a
few waterborne outbreaks (Bruce-Grey-Owen Sound Health Unit, 2000; Schuster et al., 2005;
Craun et al., 2006; Clark et al., 2010). In Canada, the Walkerton outbreak of 2000 was the first
documented outbreak of E. coli O157:H7 infection associated with a Canadian municipal water
supply and the largest multibacterial waterborne outbreak in the country to date (Bruce-GreyOwen Sound Health Unit, 2000). Surveillance reports published for other countries have
indicated that over the period from 1990 to the early 2000s, E. coli O157:H7 was identified as the
causative agent of approximately 6% of the reported drinking water outbreaks in England and
Wales (Smith et al., 2006) and roughly 7% of those reported in the United States (Craun et al.,
2006).
Cattle and human sewage are the primary and secondary sources, respectively, of EHEC
(Jackson et al., 1998; Percival et al., 2004; Gyles, 2007), but human sewage is the major source
of the other pathogenic E. coli groups (Percival et al., 2004; AWWA, 2006). Transmission of
pathogenic E. coli occurs through the faecal–oral route, and the primary routes of exposure are
from contaminated food or water or by person-to-person transmission (Percival et al., 2004;
AWWA, 2006). Pathogenic E. coli are not usually a concern in treated drinking water when
treatment and distribution systems are properly operated and maintained. However, outbreaks of
E. coli O157:H7 involving consumption of drinking water contaminated with human sewage or
cattle faeces have been documented in North America (Olsen et al., 2002), including some fatal
outbreaks (Swerdlow et al., 1992; Novello, 1999; Bruce-Grey-Owen Sound Health Unit, 2000).
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The probability of becoming ill depends on the number of organisms ingested, the health status of
the person and the resistance of the person to the organism or toxin (LeChevallier et al., 1999).
With the exception of EHEC, most pathogenic E. coli require a high number of bacteria to
be ingested in order to produce illness. Infectious dose estimates for non-EHEC strains range
from 105 to 1010 organisms (Percival et al., 2004). EHEC strains, in contrast, have a very low
infectious dose. It has been suggested that ingestion of fewer than 100 cells may be sufficient to
cause infection (Percival et al., 2004; Pond, 2005). The onset and duration of pathogenic E. coli–
related illness will be strain dependent, but symptoms can begin in as little as 8–12 hours and last
from a few days up to a few weeks (Percival et al., 2004).
Pathogenic E. coli can cause diarrhoea that ranges in severity from mild and self-limiting
to severe and life-threatening (Percival et al., 2004; AWWA, 2006). Most non-EHEC illness is
marked by a watery diarrhoea that can be accompanied by vomiting, abdominal pain, fever and
muscle pain, depending on the group or strain involved.
EHEC illness can begin with watery and bloody diarrhoea in combination with vomiting,
but in some cases can progress to the more serious and potentially life-threatening symptoms of
haemorrhagic colitis (grossly bloody diarrhoea) and haemolytic uraemic syndrome (kidney
failure). These symptoms are caused by shiga-like toxins, potent toxins that are related to
Shigella dysenteriae toxins (Percival et al., 2004; AWWA, 2006). It has been suggested that up to
10% of E. coli O157:H7 infections can progress to haemolytic uraemic syndrome (Moe, 1997;
Sherman et al., 2010). Children and the elderly are most susceptible to the complications that
arise from EHEC infections (Percival et al., 2004). One area of recent interest has been the
possible long-term health effects in adults as a result of contracting haemolytic uraemic syndrome
from E. coli O157:H7, as these to date have been largely unknown (Clark et al., 2010). Clark et
al. (2010) reported on the results of a health study among persons who developed gastrointestinal
illness or remained asymptomatic following exposure to E. coli O157:H7 and Campylobacter
during the Walkerton outbreak in May 2000. The authors concluded that increases in the
incidences of hypertension, cardiovascular disease and indicators of kidney impairment were
evident in persons who experienced acute gastroenteritis during the outbreak. Further study in
this area is required, but because such waterborne outbreaks are rare, there are very limited
opportunities for such studies.
B.1.1.1 Treatment technology
In the majority of treatment and disinfection studies involving pathogenic E. coli, the
EHEC strain O157:H7 has been selected as the model organism because of its health significance
and prominence in foodborne and waterborne outbreaks. Regardless, review of the evidence
generated to date suggests that the proper application of water treatment and disinfection
technologies will be capable of controlling strains of pathogenic and non-pathogenic E. coli in
drinking water (Percival et al., 2004; AWWA, 2006).
In terms of chlorine and monochloramine effectiveness, laboratory studies have
demonstrated E. coli O157:H7 log inactivation capabilities of up to 4 log at concentrations and
contact times that would be encountered in municipal drinking water treatment (Rice, 1999;
Wojcicka et al., 2007; Chauret et al., 2008).
For ultraviolet (UV) disinfection, Zimmer-Thomas et al. (2007) observed log
inactivations of 4.5 log or greater for E. coli O157:H7 at all tested doses of low-pressure and
medium-pressure UV. These included UV doses commonly used in water disinfection (20 and 40
mJ/cm2, low pressure), as well as low doses intended to be representative of compromised UV
dose delivery (5 and 8 mJ/cm2, low and medium pressure). In UV inactivation experiments,
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Sommer et al. (2000) observed considerable divergence in sensitivity of different pathogenic
(including enterohaemorrhagic) strains of E. coli. The authors further demonstrated that a UV
dose of 125 J/m2 (equivalent to 12.5 mJ/cm2) was sufficient to produce a 6 log inactivation of all
of the strains under study.
Further information on treatment technologies for E. coli can be found in the E. coli
guideline technical document (Health Canada, 2012).
B.1.1.2 Assessment
Studies have shown that the survival and susceptibility to disinfection of pathogenic E.
coli strains approximate those of typical E. coli (LeChevallier et al., 1999; Rice, 1999). Also,
although routine examination methods for E. coli are not designed to distinguish pathogenic E.
coli strains from the general E. coli population, the latter will always occur in greater
concentration in faeces, even during outbreaks. Pathogenic E. coli will not occur in the absence
of generic E. coli. As a result, the presence of E. coli is the best available indicator of faecal
contamination and the potential presence of faecal pathogens, but is not a specific signal for the
presence of pathogenic E. coli.
B.1.2 Salmonella and Shigella
Salmonella and Shigella are agents of gastrointestinal illness that belong to the same
microbiological family as E. coli, Enterobacteriaceae.
Salmonella are non-spore-forming, facultative anaerobic, Gram-negative bacilli that are
2–5 µm long and 0.8–1.5 µm wide (AWWA, 2006). Salmonella is a complex taxonomic genus
consisting of over 2000 different varieties or serological types that can cause infections in
animals and humans (AWWA, 2006). According to experts, the genus is officially made up of
only two species, Salmonella enterica and Salmonella bongori (Percival et al., 2004; AWWA,
2006). Salmonella enterica is the species of most relevance for human infections, and it can be
further broken down into six subspecies, of which one, Salmonella enterica subsp. enterica,
contains the majority of serotypes that are associated with cases of human gastroenteritis
(Percival et al., 2004). By convention, when referring to Salmonella serotypes, the serotype is
adopted as the species name (e.g., Salmonella enterica subsp. enterica serovar enteritidis
becomes Salmonella enteritidis).
The vast majority of Salmonella serotypes encountered in developed countries are
zoonotic pathogens. Reservoirs for these organisms include poultry, pigs, birds, cattle, cats, dogs,
rodents and turtles (AWWA, 2006). Infected humans and, as a result, sewage are also sources of
Salmonella. Transmission of Salmonella occurs through the faecal–oral route, predominantly
through food. By comparison, drinking water is not often implicated as a source of Salmonella
infection (Percival et al., 2004). As Salmonella is a zoonotic pathogen, runoff from agricultural
lands can provide a mechanism for the transfer of animal faecal wastes to source waters.
Shigella are facultative anaerobic, non-sporulating, non-motile, Gram-negatives rods 0.3–
1.5 µm in diameter and 1–6.5 µm in length (AWWA, 2006). The taxonomy of Shigella is much
simpler than that of Salmonella. The genus is categorized into four major serological groups:
dysenteriae, flexneri, boydii and sonnei. Shigella sonnei and Shigella flexneri are the two species
of importance as causes of gastrointestinal illness in developed countries (Percival et al., 2004).
Infected humans are the only significant reservoir (AWWA, 2006). Transmission is faecal–oral,
through drinking water or through food that has been contaminated with human faecal wastes.
Person-to-person transmission is also a significant route of exposure for Shigella, particularly
among children. Shigella is a human-specific pathogen and is not expected to be found in the
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environment (AWWA, 2006). Thus, contamination of water supplies is suggestive of a source of
human faecal contamination, such as from sewage or on-site wastewater disposal systems.
Numerous outbreaks linked to contaminated drinking water have been reported
worldwide (Boring et al., 1971; White and Pedersen, 1976; Auger et al., 1981; Arnell et al., 1996;
Angulo et al., 1997; Alamanos et al., 2000; R. Taylor et al., 2000; Chen et al., 2001). Schuster et
al. (2005) reported that Shigella and Salmonella were identified as the causative agents in 9 and
16 confirmed, proposed or suspected drinking water outbreaks in Canada, respectively, over the
years 1974–2001. In the United States, Salmonella and Shigella accounted for approximately 2%
and 5% of drinking water outbreaks reported from 1991 to 2002, according to U.S. surveillance
data (Craun et al., 2006). Common causes of waterborne outbreaks by these organisms are poor
source water, inadequate treatment or post-treatment contamination (e.g., by cross-connections)
(AWWA, 2006). Both organisms give rise to acute, self-limiting gastrointestinal illness with
symptoms of diarrhoea, vomiting and abdominal pain. Shigella-associated illness is more
dysenteric in nature, marked by a more watery diarrhoea containing blood and mucus (AWWA,
2006). Once infected, recovering individuals may continue to shed either of these organisms in
their faeces for days up to several weeks or months. Published reports regarding the median
infective doses for these two organisms have suggested that they may be as low as 103–105
organisms for Salmonella serotypes and 102–103 organisms for Shigella flexneri and Shigella
sonnei (Hunter, 1997; Kothary and Babu, 2001). The factors that contribute to the virulence of
these organisms are still under investigation. Both possess mechanisms that enable the bacteria to
invade, survive, replicate and disrupt the function of the human intestinal lining (Percival et al.,
2004). In addition, Shigella sonnei and Shigella flexneri are known to produce an exotoxin that
affects intestinal water absorption and retention (Percival et al., 2004).
B.1.2.1 Treatment technology
Salmonella and Shigella survival characteristics in water and their susceptibility to
disinfection have been demonstrated to be similar to those of coliform bacteria, including E. coli
(McFeters et al., 1974; Mitchell and Starzyk, 1975; Chang et al., 1985; Koivunen and HeinonenTanski, 2005). It is generally recognized that a properly operated facility will be sufficient in
controlling Salmonella and Shigella in treated drinking water (AWWA, 2006).
B.1.2.2 Assessment
The absence of E. coli during routine verification should be an adequate indication of the
sufficient removal and inactivation of Salmonella and Shigella.
B.1.3 Campylobacter and Yersinia
Campylobacter are pathogenic bacteria found primarily in the intestinal tracts of domestic
and wild animals, especially birds. Poultry, cattle, sheep and pigs are considered significant
reservoirs for these organisms (Percival et al., 2004; AWWA, 2006). Campylobacter are motile,
Gram-negative, slender, curved rods 0.2–0.5 µm wide and 0.5–5 µm long. Yersinia can be found
in the faeces of wild animals as well as domestic livestock such as cattle, pigs and sheep (Percival
et al., 2004). Yersinia are facultative anaerobic, Gram-negative, non-sporulating rods 0.5–0.8 µm
in diameter and 1–3 µm in length (AWWA, 2006). It is the Campylobacter species C. jejuni, C.
coli and C. upsaliensis and the Yersinia species Y. enterocolitica that are most important to the
water industry (AWWA, 2006). Human sewage also contains large numbers of both of these
organisms.
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Both Campylobacter and Yersinia enterocolitica are transmitted through the faecal–oral
route, mostly through contaminated food and sometimes through water (Percival et al., 2004).
Person-to-person transmission of Campylobacter or Yersinia enterocolitica is uncommon
(Percival et al., 2004; AWWA, 2006).
Waterborne outbreaks of gastroenteritis involving Campylobacter jejuni and Yersinia
enterocolitica have been recorded on numerous occasions, with improper treatment, posttreatment contamination or consumption of untreated water supplies being the most frequent
causes (Eden et al., 1977; McNeil et al., 1981; Mentzing, 1981; Vogt et al., 1982; Taylor et al.,
1983; Lafrance et al., 1986; Sacks et al., 1986; Thompson and Gravel, 1986). In a review of
Canadian data on waterborne outbreaks for the period spanning from 1974 to 2001, Schuster et
al. (2005) reported that Campylobacter was implicated in 24 outbreaks and was second only to
Giardia (51 outbreaks) in outbreaks where a causative agent was identified. The most notable
Canadian waterborne outbreak was the May 2000 Walkerton outbreak involving Campylobacter
and E. coli O157:H7, where faecally contaminated well water was not properly treated before
consumption (Clark et al., 2003). No outbreaks of Yersinia-related gastroenteritis have been
reported for municipal drinking water supplies in North America over the past two decades
(Schuster et al., 2005; Craun et al., 2006).
Gastroenteritis caused by Campylobacter typically presents as flu-like symptoms and/or
abdominal pain, followed by a profuse watery diarrhoea caused by the presence of an enterotoxin
similar to cholera toxin (AWWA, 2006). An important characteristic of Campylobacter is the
high infectivity potential; as few as 1000 organisms can cause infection (Black et al., 1988; HaraKudo and Takatori, 2011). Yersinia enterocolitica can cause a variety of symptoms, depending
on the age of the person infected, but the most commonly observed are gastrointestinal illness,
fever and occasionally vomiting in children (AWWA, 2006). The gastrointestinal illnesses caused
by both organisms are considered to be self-limiting (Percival et al., 2004).
B.1.3.1 Treatment technology
Studies have demonstrated the susceptibility of Campylobacter species and Yersinia
enterocolitica to disinfectants commonly used in water treatment (Blaser et al., 1980; Wang et
al., 1982; Sobsey, 1989; Lund, 1996; Rose et al., 2007). It is generally recognized that treatment
technologies effective in the removal and inactivation of E. coli will be effective against these
pathogenic bacteria (AWWA, 2006).
B.1.3.2 Assessment
Studies have suggested a lack of a correlation between indicator organisms (e.g., E. coli,
total coliforms) and the presence of Campylobacter and Yersinia in raw surface water supplies
(Carter et al., 1987; Lund, 1996; Hörman et al., 2004). Thus, E. coli may not be an adequate
indicator of the presence of both C. jejuni and Y. enterocolitica in source waters at all times.
However, as it is expected that properly operated treatment and disinfection technologies are
effective in controlling these organisms in treated drinking water, it is expected that the E. coli
guideline is sufficiently protective against their potential presence.
B.2
Waterborne non-faecal pathogens
Although E. coli is the best available indicator of recent faecal contamination, there are
waterborne illnesses that result from pathogens not transmitted by the faecal–oral route. These
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pathogens are usually bacteria naturally found in source waters. Those that clearly have a public
health impact include Legionella, Mycobacterium avium complex, Aeromonas and Helicobacter
pylori. The detection of faecal indicators does not provide any information on the potential
presence of non-faecal pathogens. No indicators are currently known for such pathogens.
B.2.1 Legionella
Legionellae are recognized human pathogens that can cause two different types of illness:
Legionnaires’ disease, which is a serious respiratory illness involving pneumonia, and Pontiac
fever, which is a milder flu-like illness without pneumonia. Legionellae are free-living aquatic
bacteria that occur widely in water environments. The presence of Legionella is more of a
concern for water systems beyond municipal water treatment and distribution systems, such as
cooling towers and hospital and residential plumbing systems. Legionella species exhibit a
number of survival properties that make them relatively resistant to the effects of chlorination and
elevated water temperatures. The organisms are also capable of colonizing drinking water
distribution system biofilms (Lau and Ashbolt, 2009).
The bacteria themselves are weakly Gram-negative, small, motile rods that have precise
nutritional requirements and as a result do not grow well on culture media. At least 50 different
Legionella species have been identified, and approximately half of these species have been
associated with disease. Legionella pneumophila (serogroup 1) is the agent responsible for most
cases of illness in humans. Other than L. pneumophila, species causing far fewer infections but
still considered to be clinically relevant include L. micdadei, L. bozemanii, L. longbeachae and L.
dumoffi (Reingold et al., 1984; Doyle and Heuzenroeder, 2002; Roig et al., 2003).
B.2.1.1 Sources and exposure
Legionella species are naturally present in a wide range of freshwater environments,
including surface water (Fliermans et al., 1981; Palmer et al., 1993) and groundwater (Brooks et
al., 2004; Costa et al., 2005). The bacteria are not considered to be enteric pathogens and are not
transmitted via the faecal–oral route. However, Legionella can occasionally be detected in human
faecal samples, as diarrhoea is a symptom of illness in a small percentage of cases (Rowbotham,
1998). Similarly, animals are not reservoirs for Legionella (U.S. EPA, 1999a).
Legionella can be isolated from human-made systems (e.g., cooling towers, hot water
tanks, showerheads, aerators) and are most frequently associated with biofilms (Lau and Ashbolt,
2009). In general, the amount of legionellae in source waters is low compared with the
concentrations that can be reached in human-made systems (Mathys et al., 2008). In an
investigation of biofilm formation and Legionella colonization on various plumbing materials
(Rogers et al., 1994), the detection of Legionella was greater in biofilm than in free water but
varied in time and with different plumbing materials. Biofilms are important for the survival of
the fastidious legionellae: they provide protection to Legionella, which are also able to utilize
nutrients supplied by other organisms in this nutrient-rich environment (Borella et al., 2005;
Temmerman et al., 2006; Lau and Ashbolt, 2009).
Some naturally occurring waterborne protozoa, such as Acanthamoeba, Hartmanella,
Naegleria, Valkampfia and Echinamoeba, can also harbour Legionella organisms (Rowbotham,
1986; Kilvington and Price, 1990; Kramer and Ford, 1994; Fields, 1996). Legionella can infect
and remain within the protozoan cyst form, where they are protected from disinfectants
(Kilvington and Price, 1990; Thomas et al., 2004; Declerck et al., 2007). They are also able to
multiply within these protozoa, which has been proposed as the only way that Legionella can
replicate within aquatic systems (Abu Kwaik et al., 1998; Thomas et al., 2004). Thus, as well as
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offering protection, this association suggests a mechanism for the increase and transport of L.
pneumophila in human-made systems (Declerck et al., 2009).
Temperature is an additional factor that influences Legionella colonization of water
systems. Temperatures between 20°C and 50°C are hospitable for colonization, although
legionellae typically grow to high concentrations only at temperatures below 42°C (Percival et
al., 2004).
Plumbing systems outside of public water supply systems (e.g., in residential buildings,
hotels, institutional settings) are most commonly implicated in L. pneumophila infections (Yoder
et al., 2008). As Legionella is a respiratory pathogen, systems that generate aerosols, such as
cooling towers, whirlpool baths and showerheads, are the more commonly implicated sources of
infection. The hot water supply system is commonly pinpointed as the origin of the
contamination (Hershey et al., 1997; McEvoy et al., 2000; Borella et al., 2004; Oliver et al.,
2005; Burnsed et al., 2007; Yoder et al., 2008). However, the cold water supply, when held at
about 25°C, which is within the range of Legionella multiplication, has also been implicated
(Hoebe et al., 1998; Cowgill et al., 2005). Legionella infection can occur when people breathe in
aerosolized water containing the bacteria or aspirate water containing the bacteria. The bacteria
have not been found to be transmitted from person to person (U.S. EPA, 1999a).
Legionella contamination is particularly troublesome in hospitals, where susceptible
individuals can be exposed to aerosols containing hazardous concentrations of L. pneumophila.
Large buildings such as hotels, community centres, industrial buildings and apartment buildings
are most often implicated as sources of outbreaks (Reimer et al., 2010). Studies have shown that
contamination of domestic hot water systems with Legionella can occur in single-family homes
(Joly, 1985; Alary and Joly, 1991; Stout et al., 1992a; Marrie et al., 1994; Dufresne et al., 2012).
In a study of hot water plumbing systems in homes in the Québec area, Alary and Joly (1991)
reported that Legionella was detected in 39% (69/178) of hot water tanks with electric heaters
and in 0% (0/33) of tanks with oil- or gas-fired heaters. The authors further observed that in a
proportion of those homes whose hot water tanks tested positive for Legionella, the organism
could also be detected at distal locations, such as faucets (12%) and showerheads (15%). The
position of the heat source in the design of electrically heated hot water tanks observed at the
time of the study was cited as the reason for the difference in contamination between the two
water heater types. In the electric tanks, the heating elements were located above the bottom of
the heater, which could allow bottom sediments and water below the heating element to remain at
the lower temperatures (< 50–60°C) permissible for Legionella growth (Alary and Joly, 1991).
Although the presence of the bacteria in the home can increase the risk of infection in susceptible
individuals, it does not necessarily mean that occupants will develop the illness. In addition,
although outbreaks generally do not occur in residential settings, individual cases have been
identified as originating from residential plumbing (Falkinham et al., 2008).
Similarly, evidence has been provided that sporadic cases of Legionnaires’ disease can
plausibly be acquired from aerosols in residential plumbing systems (Stout et al., 1992b; Straus et
al., 1996; Lück et al., 2008). In a study conducted in the province of Quebec, Dufresne et al.
(2012) observed that among 36 legionellosis-confirmed patients residing in homes with domestic
hot water tanks, residential and clinical isolates of Legionella were microbiologically related by
pulse-field gel electrophoresis in 14% (5/36) of the cases. Similar studies conducted in
Pittsburgh, Pennsylvania (Stout et al., 1992b), and the state of Ohio (Straus et al., 1996) showed
comparable results.
Persons thought to be at the highest risk of contracting Legionnaires’ disease are those
with lung conditions or compromised immune systems (e.g., persons receiving transplants or
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chemotherapy, persons with diabetes or kidney disease). The risk of infection is higher among
persons 40–70 years of age, and the disease is seen more frequently in males than in females
(Percival et al., 2004). Other risk factors include smoking and excessive use of alcohol.
Legionnaires’ disease is considered a very rare cause of pneumonia in children. In contrast, age,
gender and smoking do not seem to be risk factors for Pontiac fever (Diederen, 2008).
The concentration of Legionella required to cause infection is not well understood
(Armstrong and Haas, 2008). It has been suggested that amoebae harbouring Legionella may
increase the potential for infectivity by providing a mechanism to expose humans to hundreds of
Legionella cells if inhaled or aspirated in an aerosol (Rowbotham, 1986; Greub and Raoult,
2004).
B.2.1.2 Health effects
As mentioned previously, there are two distinct illnesses caused by Legionella:
Legionnaires’ disease and Pontiac fever. Collectively, these illnesses are referred to as
legionellosis. Legionnaires’ disease is a serious respiratory illness involving pneumonia. Other
features include fever, cough and headache, chest and muscle pain, and a general feeling of
unwellness (malaise) (Fields et al., 2002). The time from the point of infection to the onset of
symptoms is about 2–10 days, and the disease period can last up to several months. One problem
in diagnosing Legionnaires’ disease is a lack of any specific symptom that distinguishes it from
other bacterial pneumonias. Reported rates of Legionnaires’ disease in Canada over the period
2000–2004 (the latest year for which data have been published) ranged from 0.13 to 0.20 cases
per 100 000 population (PHAC, 2006). The mortality rate of Legionnaires’ disease in the United
States as of 1998 was reported at roughly 10% and 14% for community-acquired and hospitalacquired cases, respectively (Benin et al., 2002). Early diagnosis and antibiotic therapy are keys
to successfully treating Legionnaires’ disease.
Pontiac fever is a less serious respiratory illness that does not involve pneumonia and is
more flu-like in nature. The time to the onset of symptoms is 24–48 hours (AWWA, 2006). The
disease is self-limiting and typically resolves without complications in 2–5 days. No known
fatalities have been reported with this illness. Pontiac fever is difficult to distinguish from other
respiratory diseases because of a lack of specific clinical features. Experts have speculated that
the disease may be caused by exposure to a mixture of live and dead Legionella cells and nonLegionella endotoxin (Diederen, 2008). Antibiotic treatment is typically not prescribed because
of the short, self-limiting nature of the disease.
B.2.1.3 Treatment technology
Successful control of Legionella in drinking water supplies requires focused attention not
only on the organisms themselves, but also on the control of free-living amoebae and biofilms
that support their persistence.
Physical removal mechanisms used during drinking water treatment, such as conventional
filtration (i.e., coagulation, flocculation and sedimentation), will reduce the number of Legionella
present in finished water. Disinfection strategies shown to be effective in reducing the number of
Legionella present include the use of chlorine, monochloramine, chlorine dioxide ozone and UV.
However, it must be noted that chlorine dioxide (Health Canada, 2008) and ozone (U.S. EPA,
1999b) are generally not effective in maintaining a disinfectant residual in the distribution system
and UV does not provide a disinfectant residual. In comparison with E. coli, Legionella cells
have been shown to be more resistant to chlorination (Delaedt et al., 2008; Wang et al., 2010).
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Survival strategies exhibited by the organisms (colonization of biofilms and residence within
free-living amoebae) also further protect Legionella from the action of disinfectants.
In the distribution system, currently recommended disinfectant residuals are sufficient to
keep the concentration of non-biofilm-associated Legionella at levels that have not been
associated with disease (Storey et al., 2004; Delaedt et al., 2008).
Various alternative disinfection methods have been examined for their potential to control
Legionella colonization in municipal drinking water distribution systems. Monochloramine has
been shown to be more effective than chlorine as a residual disinfectant against legionellae.
Weintraub et al. (2008) observed that converting from chlorine to monochloramine for residual
disinfection in a municipal distribution system resulted in a significant reduction in the number of
distribution samples, point-of-use sites and water heaters positive for Legionella colonization.
Pryor et al. (2004) studied the impact of changing the secondary disinfectant from chlorine to
chloramine on the microbiological quality of the drinking water in a utility. Samples were taken
from the source water, from the distribution system and at the point of use (i.e., showerheads).
The authors found that there was a decrease in the colonization rate and the variety of Legionella
species present in samples from the distribution system and showerheads when the disinfectant
was changed from chlorine to choramine. However, despite the decrease in the variety of
Legionella species, there was no indication of a decrease in L. pneumophila at the point of use
(Pryor et al., 2004).
Kool et al. (1999) reported that hospitals supplied with water containing monochloramine
for secondary disinfection were less likely to have reported outbreaks of Legionnaires’ disease
than those supplied with water containing free chlorine. Monochloramine is considered better
able to penetrate into biofilms (LeChevallier et al., 1980), more stable and therefore able to
maintain its concentration over greater distances in the distribution system (Kool et al., 1999).
It has been suggested that ozone may be a more effective disinfectant against Legionella
than chlorine, but its main drawback is that it does not provide a disinfectant residual (U.S. EPA,
1999b; Kim et al., 2002; Blanc et al., 2005). Loret et al. (2005) observed that ozone at a
concentration of 0.5 mg/L was effective in reducing Legionella, protozoa and biofilms in a model
distribution system, but it was not as effective as chorine (2 mg/L) or chlorine dioxide (0.5
mg/L). Conversely, ozone at a concentration of 0.1–0.3 µg/mL (0.1–0.3 mg/L) was shown to be
as effective as free chlorine at 0.4 mg/L in inactivating Legionella suspensions, producing a 2 log
reduction of the organism within 5 minutes in laboratory experiments (Dominique et al., 1988).
There are also a variety of supplemental strategies that can be used to control Legionella in the
plumbing systems of large commercial, industrial and residential buildings.
Hyperchlorination has been employed as a control strategy in large buildings, including
hospitals. However, studies have demonstrated that Legionella residing in biofilms or in cysts of
Acanthamoeba polyphaga can survive following exposure to free chlorine at 50 mg/L
(Kilvington and Price, 1990; Cooper and Hanlon, 2010). There is also the concern of an increased
potential for corrosion of plumbing systems with continued high concentrations of chlorine (Kool
et al., 1999).
Chlorine dioxide has demonstrated similar advantages over chlorine as a residual
disinfectant for Legionella control when applied to a small distribution system such as a hospital
complex. Sidari et al. (2004) observed significantly decreased Legionella concentrations at hot
and cold point-of-use sites of a hospital’s plumbing system upon switching to chlorine dioxide as
the residual disinfectant.
In plumbing systems of hospitals and large buildings, thermal disinfection (elevating hot
water to temperatures above 70°C, and flushing use points such as taps and showerheads) has
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been routinely employed either on its own or in conjunction with chemical disinfection. Typically
this is recognized as a temporary control strategy, as Legionella recolonization can occur within
weeks to months of treatment (Storey et al., 2004).
Use of copper–silver ionization systems has also received much study and has shown
effectiveness in controlling Legionella in drinking water supplies (Stout et al., 1998; Kusnetsov
et al., 2001; Stout and Yu, 2003; Cachafeiro et al., 2007). Stout et al. (1998) observed that
copper–silver ionization (mean copper and silver concentrations of 0.29 mg/L and 0.054 mg/L,
respectively, in the hot water tank) was more effective than a superheat-and-flush method in
reducing the recovery of Legionella from a hospital plumbing/distribution system. In a survey of
the experiences of hospital systems using copper–silver ionization, Stout and Yu (2003) reported
that following installation of the disinfection systems, the percentages of hospitals reporting (1)
cases of Legionnaires’ disease and (2) positive Legionella samples at more than 30% of the sites
measured had both been reduced to 0% from 100% and 47%, respectively, before the systems
had been installed. It is important to note that use of these systems should include monitoring of
copper and silver concentrations in the water, as these concentrations will increase. In addition,
pretreatment may be required to address pH and hardness challenges (Bartram et al., 2007).
Additional measures used for large plumbing systems include temperature control; control
of water system design and construction to prevent the accumulation of biofilms, sediments or
deposits; and nutrient control strategies (Bartram et al., 2007; Bentham et al., 2007).
General recommendations regarding the control of Legionella in domestic plumbing
systems involve maintaining proper water temperatures. The National Plumbing Code of Canada
includes requirements of a minimum water temperature of 60°C in hot water storage tanks, to
address the growth of Legionella (NRCC, 2010). Where increased hot water temperatures create
an increased risk of scalding for vulnerable groups (e.g., children and the elderly), appropriate
safety measures should be applied to limit the temperature to 49°C. Thermostatic or pressurebalanced mixing valves can be installed to control the water temperature at the tap to reduce the
risk of scalding (Bartram et al., 2007; Bentham et al., 2007).
Control of Legionella in water systems outside of plumbing systems also requires
controlling its growth in biofilms. The heating, ventilation and air conditioning industry has
guidelines for reducing Legionella growth in cooling systems (ASHRAE, 2000). Hotel and
lodging industry requirements for the operation and maintenance of plumbing facilities, including
procedures for the proper disinfection of plumbing equipment in their facilities, are generally
specified under various public health regulations and/or legislation. To obtain information on
these requirements, the appropriate provincial or territorial ministry of health should be
consulted.
B.2.1.4 Assessment
The increasing importance of Legionella as a cause of human infection can in part be
linked to continued human development and the resulting dependence on human-made plumbing
systems (Fields et al., 2002). Despite being ubiquitous in source waters, Legionella pneumophila
and other Legionella species have been recovered only in low concentrations from Canadian
drinking water supplies (Dutka et al., 1984; Tobin et al., 1986), and people do not get infected
with Legionella by consuming drinking water. As Legionella is a respiratory pathogen, infection
can occur if people breathe in contaminated aerosols. Thus, the presence of Legionella becomes a
problem only when they are able to grow to high numbers in water systems such as showers,
cooling towers or whirlpool baths that generate aerosols or sprays. These plumbing systems have
been implicated in outbreaks, but are mainly outside of the control of municipal water treatment
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and distribution. For these reasons, the presence of the organism in low numbers in the
distribution network is not sufficient evidence to warrant remedial action in the absence of
disease cases (Dufour and Jakubowski, 1982; Tobin et al., 1986).
Owing to the existence of Legionella outside of faecal sources in nature, E. coli is not
expected to be a reliable indicator of the presence of these bacteria. No suitable indicators have
been identified to signal increasing concentrations of Legionella in a building’s plumbing system.
There is some evidence that increasing Legionella concentrations are accompanied, or preceded,
by elevated heterotrophic plate count (HPC) measurements (WHO, 2002). However, the
correlation between HPC and Legionella is not consistent.
Legionella have also been included on the U.S. Environmental Protection Agency’s
(EPA) Candidate Contaminant List as one of the priority contaminants for regulatory decisionmaking and information collection (U.S. EPA, 2009). Guidelines or regulations that have been
developed for Legionella in Canada, the United States and other countries worldwide relate to
control of the organism in water environments outside of municipal water distribution networks
(e.g., piped water systems, cooling towers, health care facilities) (Cunliffe, 2007).
B.2.2 Mycobacterium avium complex
The Mycobacterium avium complex (Mac)1 is a group of environmental mycobacteria that
can cause illness in humans. The group consists of Mycobacterium avium (includes subspecies
avium, sylvaticum and paratuberculosis); and Mycobacterium intracellulare (Cangelosi et al.,
2004). Mac organisms are considered ubiquitous in natural waters. Transmission is primarily
through contact with contaminated waters via either ingestion or inhalation (AWWA, 2006).
Mac-related disease comes mainly in the form of lung infections and occurs largely in persons
who have suppressed immune systems (Percival et al., 2004).
Mycobacteria themselves are motile, rod- to coccoid-shaped bacteria that have
characteristically high levels of waxy lipids in their cell walls. They are Gram negative, but are
more commonly considered to be “acid-fast” because of the way their cell walls respond to
diagnostic staining procedures (AWWA, 2006). Mac organisms are also referred to as “nontuberculous” or “atypical” mycobacteria. This is to distinguish them from the more well-known
mycobacteria species that are responsible for tuberculosis and leprosy, which are not a concern
for drinking water (Nichols et al., 2004). Other environmental mycobacteria are known that have
been linked to skin infections through waterborne contact, but these are also of lesser importance
to drinking water supplies (Nichols et al., 2004).
B.2.2.1 Sources and exposure
Mac organisms are natural inhabitants of water and soil environments (Falkinham, 2004).
Water is considered the main reservoir (Percival et al., 2004; Vaerewijck et al., 2005), and the
organisms can be encountered in natural aquatic systems worldwide, including marine waters and
freshwater lakes, streams, ponds and springs (Falkinham, 2004; Percival et al., 2004). Mac
organisms can be encountered in drinking water supplies, but generally in low numbers and at
low frequency (Peters et al., 1995; Covert et al., 1999; Falkinham et al., 2001; Hilborn et al.,
2006). However, Mac bacteria can survive in distribution system biofilms and grow there to
1
For the purpose of this document, the acronym Mac will be used for Mycobacterium avium complex instead of the
usual MAC to avoid confusion with maximum acceptable concentration (MAC).
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reach significant populations (Falkinham et al., 2001). Counts of M. intracellulare in biofilms
were observed to reach 600 colony-forming units (CFU) per square centimetre, on average
(Falkinham et al., 2001). Feazel et al. (2009) observed that mycobacteria were enriched in
plumbing system (showerhead) biofilms, reaching counts 100 times, based on higher numbers of
genes being sequenced, above those in water samples. In another study, Tsintzou et al. (2000)
observed a statistically significant decrease in the presence of environmental mycobacteria in
drinking water samples after the replacement of the city’s water distribution network. The authors
attributed the reduction to the absence of distribution system biofilms (Tsintzou et al., 2000).
Surveys of water samples from water treatment plants and residential dwellings have reported
Mac isolation rates of 2–60% (von Reyn et al., 1993; Glover et al., 1994; Peters et al., 1995;
Covert et al., 1999; Hilborn et al., 2006). Hilborn et al. (2006) recovered M. avium from roughly
50–60% of point-of-use samples (cold water taps) served by two water treatment plants.
Concentrations ranged from 200 to > 300 CFU/500 mL (Hilborn et al., 2006). Von Reyn et al.
(1993) isolated Mac organisms from 17–25% of water supply samples collected from hot water
taps at patient care facilities (hospitals and clinics).
Other studies have reported a failure to isolate Mac organisms from water systems,
instead detecting only other non-Mac mycobacteria (von Reyn et al., 1993; Le Dantec et al.,
2002a; September et al., 2004; Sebakova et al., 2008). It has been suggested that the likelihood of
exposure to Mac bacteria in water is diverse in various areas of the world, but, in general, may be
less in developing countries (von Reyn et al., 1993; September et al., 2004). Mac organisms in
biofilms have also been found in other human-made systems, such as cooling towers (Pagnier et
al., 2009), ice machines (LaBombardi et al., 2002), nebulizer reservoirs, toilets and sinks
(AWWA, 2006) and water meters (Falkinham et al., 2001). Studies have reported the isolation of
non-tuberculous mycobacteria from groundwater, although M. avium has not been frequently
detected (Falkinham et al., 2001; Vaerewijck et al., 2005).
Similar to Legionella, the growth and survival of Mac organisms can be enhanced by their
ability to invade and survive in free-living amoebae, such as Acanthamoeba polyphaga or A.
castellanii (Cirillo et al., 1997; Steinert et al., 1998). A key difference between Mac and
Legionella, however, is that Mac organisms are able to replicate outside of amoebae, in biofilms
(Steinert et al., 1998; Vaerewijck et al., 2005).
The ubiquitous nature of Mac organisms results from their ability to survive and grow
under varied conditions. Mycobacteria can survive in water with few nutrients. Archuleta et al.
(2002) observed that M. intracellulare was capable of surviving for over a year in reverse
osmosis–deionized water. Mac organisms have also been shown to grow in natural waters over
wide ranges of pH (5–7.5), salinity (0–2%) and temperature (10–51°C) (Sniadack et al., 1992;
Falkinham et al., 2001). Water conditions that have been identified as being more favourable for
the growth of Mac organisms include high levels of humic and fulvic acids, high zinc
concentrations, low pH and low dissolved oxygen levels (Kirschner et al., 1992, 1999;
Vaerewijck et al., 2005).
Infection through contact with M. avium and M. intracellulare has been well documented
(Wendt et al., 1980; Grange, 1991; Glover et al., 1994; Montecalvo et al., 1994; von Reyn et al.,
1994; Kahana et al., 1997; Aronson et al., 1999; Mangione et al., 2001). Inhalation of
contaminated aerosols, during contact with contaminated hot tubs, spa pools or similar facilities,
is most frequently cited as the route and source of infection (Kahana et al., 1997; Mangione et al.,
2001; Rickman et al., 2002; Cappelluti et al., 2003; Lumb et al., 2004; Sood et al., 2007). Personto-person transmission of the organisms is thought to be uncommon (Falkinham, 1996; Nichols et
al., 2004). Evidence of the link between water supplies, particularly hot water supplies and Mac
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infection, has also been provided (von Reyn et al., 1994; Tobin-D’Angelo et al., 2004; Marras et
al., 2005). Von Reyn et al. (1994) reported the detection of the same strain of M. avium in
patients and hospital potable water supplies to which they had been exposed, but not in water
supplies collected from patients’ homes. Marras et al. (2005) documented a case of Macassociated hypersensitivity pneumonitis where the patient strain was recovered from the shower
and bathtub from the patient’s home, but not the hot tub. Despite these links, it has been
suggested that hospital and domestic drinking water–related cases represent a small proportion of
Mac-related illness (von Reyn et al., 1994; Phillips and von Reyn, 2001). The infectious dose of
Mac has not been well established. Rusin et al. (1997) proposed an oral infectious dose for mice
of 104–107 organisms. True estimations of the inhaled infectious dose would be dependent upon
(among other factors) the virulence of the organism and the immune status of the host.
B.2.2.2 Health effects
Mac organisms largely cause opportunistic infections in humans. Infections occur mostly
in individuals who have weakened or suppressed immune systems (e.g., patients with acquired
immunodeficiency syndrome [AIDS], the elderly or the very young) or persons with underlying
respiratory conditions, such as cystic fibrosis. Mac-related disease rarely occurs in healthy people
(Field et al., 2004). Mac organisms have low pathogenicity, so individuals can become colonized
with the organisms without exhibiting any adverse health effects.
The main symptom of Mac lung infection is a chronic productive cough (cough with
phlegm, saliva or mucus) (Field et al., 2004). Other symptoms can include fever, night sweats,
fatigue and weight loss (Percival et al., 2004). However, it has been suggested that the secondary
symptoms are less common unless the individual has extensive lung disease (Crow et al., 1957;
Field et al., 2004). In those individuals with human immunodeficiency virus (HIV) or AIDS, Mac
infection can spread to other parts of the body, including joints, skin, blood, liver and brain; the
disease can be debilitating and life-threatening for these patients (Percival et al., 2004).
The true prevalence of Mac infections is not known, as it is not a reportable illness in
Canada or the United States. Estimates of the rate of Mac-related pulmonary disease in the
United States range from 1–2 cases to 5 cases per 100 000 persons per year, based on
epidemiological studies conducted in various U.S. cities (Marras and Daley, 2002). Marras et al.
(2007) estimated the prevalence of pulmonary non-tuberculous mycobacteria in Ontario to range
from 9 to 14 positive isolations per 100 000 population over the years from 1997 to 2003. The
authors further reported that, overall, Mac organisms were isolated in roughly 60% of the cases.
Mac diseases are treatable, but the clearing of these infections can be difficult, and
treatment can have a high rate of failure (Field et al., 2004). Mycobacteria have demonstrated
strong resistance to antimicrobial agents (Daley and Griffith, 2010). Antibiotics are delivered at
high doses and often require a long administration period (e.g., several months to over a year)
(Percival et al., 2004; Daley and Griffith, 2010).
B.2.2.3 Treatment technology
Water treatment technologies commonly used, including chemical disinfection and
physical removal methods, have been tested for their ability to inactivate or remove mycobacteria
from water supplies. Of these technologies, the most effective has been physical removal using
conventional filtration (i.e., coagulation, flocculation and sedimentation). In one study,
Falkinham et al. (2001) observed that water treatment plants treating surface water sources
reduced mycobacteria numbers by 2–4 log through filtration and primary disinfection. A
significant association between the frequency of detection of M. avium and high raw water
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turbidity was also reported. The authors were careful to note that reducing turbidity could
represent one approach to reducing mycobacteria in drinking water, but that this procedure alone
may not be completely sufficient to eliminate M. avium from the distribution system (Falkinham
et al., 2001). It is important to note that even with good removal of organisms from the source
water, the number of Mac organisms may increase in the distribution system (Falkinham et al.,
2001). Mac organisms are more resistant than other microorganisms to commonly used
disinfectants. The high concentration of mycolic acid and the hydrophobic surface characteristics
of mycobacteria are primarily responsible for their high resistance to chemical disinfection
(LeChevallier, 2004).
In a study to evaluate the change in the microbiological population of a water distribution
system by changing the secondary disinfectant from chlorine to chloramine, the authors reported
the presence of mycobacteria from sites where the chlorine residual was above 3 mg/L. In this
same study, samples from the distribution system and at the point of use (i.e., showerheads) were
analyzed, and the authors reported that the colonization rate of mycobacteria in samples from the
distribution system and showerheads increased when the disinfectant was changed from chlorine
to chloramine (Pryor et al., 2004).
For chlorination, Le Dantec et al. (2002b) reported varying chlorine sensitivities among a
collection of various mycobacteria isolated from the distribution system (note: Mac organisms
were not isolated in this study). The authors calculated that a CT value of 60 mg·min/L (e.g., 0.5
mg/L for 2 hours) would result in a 1.5–4 log reduction for environmental mycobacteria. R.H.
Taylor et al. (2000) provided data on the susceptibility of environmental and patient isolates of
M. avium to various disinfectants: chlorine, monochloramine, ozone and chlorine dioxide. The
mean CT99.9 values (i.e., the CT values for a 3 log reduction) for the individual disinfectants were
51–204 mg·min/L for chlorine, 91–1710 mg·min/L for monochloramine, 0.10–0.17 mg·min/L for
ozone and 2–11 mg·min/L for chlorine dioxide. The authors did note that there was significant
variation in the susceptibility of different strains (R.H. Taylor et al., 2000).
In another study using chlorine dioxide, Vicuña-Reyes et al. (2008) reported CT99.9 values
ranging from 3 to 36 mg·min/L (5–30°C), prompting the authors to conclude that the disinfectant
can be effective in controlling mycobacteria. Compared with the CT values necessary to
inactivate E. coli, the CT values necessary for inactivation of Mac have been reported to range
from near equivalency to a few times greater (monochloramine); to tens to hundreds of times
greater (ozone, chlorine dioxide); to over 2000 times greater (chlorine) (R.H. Taylor et al., 2000).
Data have been provided suggesting that mycobacteria are more sensitive than Cryptosporidium
oocysts to chlorine, monochloramine, chlorine dioxide and ozone and are as sensitive as or more
sensitive than Giardia to all of these, with the exception of free chlorine (Jacangelo et al., 2002;
LeChevallier, 2004).
In UV disinfection studies, Hayes et al. (2008) demonstrated that patient and
environmental strains of M. avium and M. intracellulare exhibited a greater than 4 log reduction
at UV fluences less than 20 mJ/cm2. The authors concluded that Mac organisms in free
suspension could be readily inactivated by UV doses commonly employed in drinking water
treatment (Hayes et al., 2008). LeChevallier (2004) reported that UV values required to inactivate
mycobacteria are in the range of those required for other vegetative bacteria.
As stated above, there may be an increase of Mac organisms in the distribution system
relative to levels leaving the treatment plant. By residing within biofilms or free-living amoebae,
Mac organisms can further increase their resistance to inactivation. Steed and Falkinham (2006)
observed that M. avium and M. intracellulare cells in biofilms were up to 1.8–4 times more
resistant than cells in free suspension when exposed to chlorine. As with Legionella, successful
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control of Mac organisms requires control of the free-living amoebae and biofilms that support
their persistence.
Mac organisms have also demonstrated resistance to elevated temperatures. Several
authors have reported recovery of M. avium from hot water systems at temperatures between
50°C and 57°C (du Moulin et al., 1988; von Reyn et al., 1994; Covert et al., 1999; Norton et al.,
2004). Additional factors thought to play a role in encouraging growth in the distribution system
include high assimilable organic carbon levels, as well as distribution system materials and
construction (e.g., pipe materials, gaskets, coatings, corroded pipes, dead ends, spaces, long
storage times) (Falkinham et al., 2001). Similar to the distribution system control strategies
described for Legionella (Bartram et al., 2007; Bentham et al., 2007), temperature control;
control of water system design and construction to prevent the accumulation of biofilms,
sediments or deposits; and nutrient control strategies should also prove effective in the control of
Mac organisms.
B.2.2.4 Assessment
No suitable indicators have been identified to signal increasing concentrations of Mac
organisms in water systems. For example, studies have found no relationship between the
numbers of non-tuberculous mycobacteria recovered from reservoir water and coliform counts,
HPC and total and free chlorine levels (Glover et al., 1994; Aronson et al., 1999). There is some
evidence that M. avium presence is associated with turbidity in raw waters (Falkinham et al.,
2001), but further exploration of this issue is needed.
Currently, the presence of mycobacteria in water is not regulated by any country or
international organization, including Canada. The U.S. EPA has identified M. avium and M.
intracellulare as waterborne health-related microbes that need additional research on their health
effects, their occurrence in water and their susceptibility to treatment methods. These organisms
have also been included in a list of candidate contaminants for possible regulation by the U.S.
EPA (2009). At the present time, there is not sufficient information to warrant actions based on
the presence of the organisms in the absence of disease.
B.2.3 Aeromonas
The genus Aeromonas has gained public health recognition as including organisms that
can cause opportunistic infections in humans. Species of Aeromonas have been associated with
gastroenteritis; however, understanding of the role that the organisms play in causing diarrhoeal
illness is currently incomplete. Skin, wound and soft tissue infections with Aeromonas species as
a result of exposure to contaminated water in non–drinking water scenarios have been well
documented. It is believed that drinking water has the potential to serve as a route of
transmission, but direct evidence of Aeromonas as a cause of drinking water–acquired
gastrointestinal illness is lacking.
Aeromonads are Gram-negative, short, rod-shaped bacteria that share some similarities
with Vibrio and E. coli. They are universally found, occurring naturally in virtually all water
types. The genus Aeromonas contains more than 17 distinct genetic species. Three species—A.
hydrophila, A. veronii biovar sobria (syn. A. sobria) and A. caviae—account for roughly 85% of
human infections and are therefore considered to be the species of most importance for drinking
water systems (Janda and Abbott, 1998, 2010).
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B.2.3.1 Sources and exposure
Aeromonas species can be found in virtually all surface water types (freshwater, marine
and estuarine) in all but the most extreme conditions of pH, salinity and temperature (Percival et
al., 2004; AWWA, 2006). They are less frequently detected in groundwater, with their presence
in these systems typically indicating well contamination (Havelaar et al., 1990; Massa et al., 1999
Borchardt et al., 2003).
Aeromonads are recognized animal pathogens (Percival et al., 2004; AWWA, 2006). The
organisms have been isolated from the gastrointestinal tracts and infected tissues of a number of
cold-blooded and warm-blooded animals, most notably fish, birds, reptiles and domestic
livestock (U.S. EPA, 2006; Janda and Abbott, 2010). They have also been recovered from retail
food items, such as meat, poultry and dairy products (Janda and Abbott, 2010). It has been
suggested that animals may be an environmental reservoir for Aeromonas (Janda and Abbott,
2010).
The organisms are not considered to be natural faecal pathogens (U.S. EPA, 2006).
Aeromonas species are not normally found in human faeces in high numbers (Janda and Abbott,
2010); however, a small percentage of the population can carry the bacteria in their intestinal
tracts without showing symptoms of disease (von Graevenitz, 2007). The prevalence of
Aeromonas in human faecal samples worldwide has been roughly estimated to be 0–4% for
asymptomatic persons and as high as 11% for persons with diarrhoeal illness (Burke et al., 1983;
U.S. EPA, 2006; von Graevenitz, 2007; Khajanchi et al., 2010). Individual studies have observed
rates as high as 27.5% and 52.4% for asymptomatic persons and diarrhoeal illness cases,
respectively (Pazzaglia et al., 1990, 1991). Numbers of Aeromonas are much higher in sewage,
with concentrations greater than 108 CFU/mL having been reported (Percival et al., 2004).
Levels of Aeromonas in clean rivers, lakes and storage reservoirs have generally been
reported to be in the range of 1–102 CFU/mL (Holmes et al., 1996). Aeromonas concentrations in
surface waters receiving sewage contamination and nutrient-rich waters in the warmer summer
months may reach 103–105 CFU/mL (Holmes et al., 1996; U.S. EPA, 2006). Groundwaters
generally contain less than 1 CFU/mL (Holmes et al., 1996). Drinking water immediately leaving
the treatment plant typically contains concentrations in the range of < 1–102 CFU/mL (Holmes et
al., 1996; U.S. EPA, 2006; Pablos et al., 2009; Janda and Abbott, 2010) , with potentially higher
concentrations in drinking water distribution systems (Payment et al., 1988; Chauret et al., 2001;
U.S. EPA, 2006). Concentrations in individual environments can be expected to vary; however,
the organisms can survive over wide ranges of pH (5–10) and temperature (2–42°C) (Percival et
al., 2004). Water temperature is particularly important to Aeromonas growth. In temperate climes
during the warmer months of the year, the bacteria have been shown to be more readily detected
in source waters and water distribution systems (Chauret et al., 2001; U.S. EPA, 2006; Janda and
Abbott, 2010). Aeromonads are also very versatile nutritionally. They are capable of growing to
elevated numbers in water with high organic content and can also survive in low-nutrient waters
(Kersters et al., 1996).
Similar to other bacteria, Aeromonas species can enter into a viable, non-culturable state
under stressful conditions in aquatic environments. There is some debate at to what effect this
state has on a species’ viability and pathogenicity. Maalej et al. (2004) reported that cells of a
strain of A. hydrophila rendered non-culturable under marine stress conditions lost their
haemolytic and cytotoxic properties, but that these could be regained following recovery at
warmer temperatures. In contrast, Mary et al. (2002) observed that viable, non-culturable cells of
A. hydrophila lost their viability and that this could not be regained following a temperature
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upshift to 25°C. It has been suggested that survival properties may differ depending on the
species and strain of Aeromonas (Brandi et al., 1999; Mary et al., 2002).
The organisms have been detected in the distribution systems of chlorinated drinking
water supplies worldwide (Chauret et al., 2001; Emekdas et al., 2006; Långmark et al., 2007;
September et al., 2007). As with other bacterial pathogens, the formation of biofilms and the
presence of free-living amoebae have been identified as factors contributing to higher
concentrations of Aeromonas encountered in drinking water distribution systems relative to
finished water (September et al., 2007; Rahman et al., 2008). During an assessment conducted as
part of their Unregulated Contaminant Monitoring Regulations, the U.S. EPA (2002) provided
data indicating that Aeromonas could be detected in 11% of municipal systems serving more than
10 000 persons and 14% of systems serving fewer than 10 000 persons. The concentrations of
Aeromonas reported were less than 10 CFU/100 mL in 78% of the samples (U.S. EPA, 2002).
Limited studies have been conducted on Aeromonas–protozoa interactions within municipal
supplies. Rahman et al. (2008) observed that the bacteria may use the free-living amoeba
Acanthamoeba as a reservoir to improve transmission and for protection from disinfectants.
Exposure to Aeromonas species through direct contact of wounds or skin follicles with
contaminated waters has been reported for recreational-type water environments, such as lakes,
rivers, swimming pools and hot tubs (Gold and Salit, 1993; Manresa et al., 2009). Unusual water
situations brought about by floods or disaster events can be expected to create similar
opportunities for Aeromonas exposure. Wound infection with species of Aeromonas was a
problem among victims of the tsunami in Thailand as a result of exposure to contaminated
floodwaters (Hiransuthikul et al., 2005). Exposure to Aeromonas in contaminated floodwaters
was also expected among victims and rescue workers following Hurricane Katrina (Presley et al.,
2006). Person-to-person transmission of Aeromonas resulting in infection is not expected to
occur (U.S. EPA, 2006).
The evidence for acquiring Aeromonas infection through the ingestion of drinking water
is not well established, and this route of transmission is the subject of some debate (von
Graevenitz, 2007). The presence of Aeromonas in finished drinking water supplies and
distribution samples has been well documented, suggesting a possible route of transmission
(LeChevallier et al., 1980; Payment et al., 1988; Kuhn et al., 1997; Borchardt et al., 2003;
Emekdas et al., 2006; de Oliveira Scoaris et al., 2008). However, other findings have been cited
that oppose this suggestion. Epidemiological investigations have demonstrated little evidence of
direct connections between patient isolates of A. hydrophila and isolates recovered from their
drinking water supplies. Borchardt et al. (2003) observed that Aeromonas isolates were
infrequently found in stool samples of gastroenteritis patients and that those detected were not
genetically related to isolates recovered from drinking water. Additionally, researchers have cited
the virtual absence of reported outbreaks of diarrhoea against the near-universal presence of
Aeromonas in water environments as evidence supporting the transmission of these organisms by
a mechanism other than through drinking water (von Graevenitz, 2007; Janda and Abbott, 2010).
Some researchers have speculated that for many faecal isolates of Aeromonas, colonization of the
human gastrointestinal tract may only be fleeting (Janda and Abbott, 2010).
The ingested dose of Aeromonas necessary to cause gastrointestinal infections is
uncertain. Limited study has suggested that a high dose is required (U.S. EPA, 2006; Janda and
Abbott, 2010). In an early volunteer feeding study, Morgan et al. (1985) reported that only 2 of
57 individuals developed diarrhoea following ingestion of A. hydrophila strains at doses of up to
1010 CFU. It has been speculated that the concentrations required to cause illness are much higher
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than the numbers that would typically be found in treated drinking water supplies (U.S. EPA,
2006).
Recently, in a large survey of clinical and waterborne strains of Aeromonas collected
from across the United States and worldwide, Khajanchi et al. (2010) reported detecting three
isolates belonging to the A. caviae group that were genetically indistinguishable and possessed
the same virulence factors. The authors suggested that these findings provided the first evidence
of human infection and colonization by a waterborne Aeromonas strain.
B.2.3.2 Health effects
Aeromonas-associated diarrhoea has been encountered worldwide, mostly in normally
healthy persons across all age groups (Janda and Abbott, 2010). Having low stomach acidity,
receiving antimicrobial therapy and having compromised immune function (e.g., from HIV
infection or through underlying disease, especially liver disease) are thought to be associated risk
factors (Merino et al., 1995; Percival et al., 2004; von Graevenitz, 2007; Janda and Abbott,
2010). The association between Aeromonas and gastrointestinal illness is controversial (von
Graevenitz, 2007; Janda and Abbott, 2010). Case reports and a small number of foodborne
outbreaks have linked the presence of Aeromonas to cases of diarrhoeal disease (U.S. EPA, 2006;
Janda and Abbott, 2010). However, at present, no outbreaks of gastrointestinal illness have been
reported for which a strain of Aeromonas has been definitely identified as the causative agent
(Janda and Abbott, 2010). Furthermore, researchers have been unable to find an animal model in
which Aeromonas-mediated gastrointestinal illness can be replicated (U.S. EPA, 2006; Janda and
Abbott, 2010).
Where Aeromonas species have been associated with gastroenteritis, the most common
symptom is watery diarrhoea, accompanied by fever and abdominal pain (Janda and Abbott,
2010). Far less commonly, Aeromonas has been identified in association with other forms of
gastrointestinal illness, ranging from a dysenteric type of illness with bloody stools to a chronic
or subacute watery diarrhoea (Janda and Abbott, 2010). Aeromonas infections can also be
asymptomatic, with individuals shedding the bacteria in their stools, but not showing any
symptoms of disease (Percival et al., 2004).
Aeromonas species have been positively isolated from skin, wound and soft tissue
infections (Percival et al., 2004; Janda and Abbott, 2010). These can range in scope from mild
irritations (e.g., pus-filled lesions) to cellulitis (inflammation below the skin) to, in extreme cases,
necrotizing fasciitis (flesh-eating disease) (Janda and Abbott, 2010). These are often the result of
trauma or penetrating injury from occupational or recreational water exposure and are generally
seen more frequently in adults than in children. Aeromonas has also recently been implicated in
respiratory infections. However, these have been rare and have largely been caused by neardrownings or aspirations of contaminated waters unrelated to drinking water supplies (Janda and
Abbott, 2010)
Factors responsible for the pathogenicity and virulence of Aeromonas species or strains
are poorly understood. A number of potential virulence components have been identified that
would appear to enable the organisms to behave as human pathogens. These include components
such as pili, fimbriae and flagella for attachment and colonization; external lipopolysaccharides,
capsules or surface layers to assist in evading host defences; and toxins, haemolysins, proteases
and other enzymes for causing damage to host cells (von Graevenitz, 2007; Janda and Abbott,
2010). Current studies have been unable to specifically pinpoint which combination of factors
would make a strain of Aeromonas behave as an enteropathogen (Janda and Abbott, 2010).
Research has identified that a known diarrhoea-causing strain of A. hydrophila possesses four
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prospective virulence factors: two haemolysins (Act and HlyA), a heat-stable enterotoxin (Ast)
and a heat-labile enterotoxin (Alt) (Erova et al., 2008 Janda and Abbott, 2010). Despite such
findings, the role and relative significance of each remain uncertain, as studies have also found
these factors distributed among numerous clinical and environmental strains in different
combinations (Erova et al., 2008 von Graevenitz, 2007; Castilho et al., 2009; Janda and Abbott,
2010). It has been proposed that only certain subsets of Aeromonas strains have the ability to
cause disease (Janda and Abbott, 2010).
Aeromonas is not a reportable organism in North America or in most countries worldwide
(Janda and Abbott, 2010; PHAC, 2010). Of the case reports or outbreaks of Aeromonas-related
illness encountered in the literature, most have been tied to food, hospitals, travel or non-water
environments, or their causes are unknown. At present, no epidemiological evidence has been
provided linking an Aeromonas outbreak to ingestion, inhalation or skin contact with treated
drinking water supplies (U.S. EPA, 2006; von Graevenitz, 2007; Janda and Abbott, 2010).
As Aeromonas-related gastrointestinal illness is mild and self-limiting, treatment for
infection is generally not necessary. However, for other presentations of infection, antibiotic
therapy is usually implemented. Aeromonads are resistant to ampicillin and a variety of other βlactam antibiotics, including penicillin and some cephalosporins (Percival et al., 2004; Janda and
Abbott, 2010).
B.2.3.3 Treatment technology
As mentioned previously, aeromonads are ubiquitous in many water environments.
Consequently, they will be present in most source waters used for drinking water production.
Nonetheless, existing evidence indicates that current treatment and disinfection methods can
effectively remove Aeromonas from drinking water. Data from pilot-scale (Harrington et al.,
2003; Xagoraraki et al., 2004) and full-scale (Chauret et al., 2001; El-Taweel and Shaban, 2001;
Yu et al., 2008) investigations have demonstrated that well-operated conventional filtration
systems (i.e., coagulation, flocculation and sedimentation) are capable of Aeromonas removals of
up to 4 log. In a pilot-scale conventional treatment study, Xagoraraki et al. (2004) observed that
reducing filter effluent turbidity to less than 0.2 NTU resulted in A. hydrophila removals of > 3
log to just under 4 log (median: 3.5 log). Yu et al. (2008) investigated the effectiveness of
different water treatment processes in removing Aeromonas as measured using both culture-based
and real-time polymerase chain reaction (PCR) detection methods. Conventional filtration (three
full-scale plants) resulted in removals of culturable Aeromonas ranging from > 0.3 log to 4 log
(Yu et al., 2008). The authors further reported that no culturable Aeromonas could be detected
after sedimentation. Log removals as measured by real-time PCR detection correlated well with,
but were routinely lower than, those demonstrated by the culture-based detection method (Yu et
al. 2008).
For slow sand filtration, the authors examined one pilot-scale and two full-scale plants,
reporting log removals of > 1 log (> 1 log for the pilot-scale plant and > 1.8 log for the full-scale
plants). Culturable Aeromonas was not detected in samples collected post-filtration (Yu et al.,
2008). Meheus and Peeters (1989) reported similar results for slow sand filtration, observing
Aeromonas removals of 98–100%.
With membrane filtration, a full-scale plant included in the Yu et al. (2008) study
demonstrated a capability of removing culturable Aeromonas by > 3.8 log.
Aeromonads are susceptible to inactivation by disinfectants commonly used in drinking
water treatment, such as chlorine, monochloramine, chlorine dioxide, ozone and UV (Knøchel,
1991; Medema et al., 1991; Sisti et al., 1998; U.S. EPA, 2002, 2006). For chlorination, Sisti et al.
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(1998) reported Aeromonas T95 values of 5 minutes at a free chlorine concentration of 0.6 mg/L
and 68 minutes at a free chlorine concentration of 0.05 mg/L in a laboratory-scale chlorination
experiment. The authors also found Aeromonas (clinical strains) to be more susceptible to
chlorine than E. coli (clinical strains). Free chlorine concentrations of 0.14 mg/L (10°C) and >
0.5 mg/L (20–37°C) were sufficient to produce a 5 log inactivation of clinical and nosocomial
strains of Aeromonas within 5 minutes in an experiment conducted by Chamorey et al. (1999). In
contrast, de Oliveira Scoaris et al. (2008) observed that the majority of Aeromonas strains (water
and culture collection strains) were not killed after 1 minute of exposure to free chlorine at 1.2
mg/L.
Chauret et al. (2001) conducted a study at both full scale and pilot scale simultaneously to
assess the presence of Aeromonas in source water and at various sites within the treatment plant
and distribution system and to assess biofilm formation. The authors noted no detectable
Aeromonas in treated water immediately after secondary disinfection with chloramine (dose
range: 2–3 mg/L), despite observing counts ranging from < 1 to 490 CFU/100 mL after chlorine
disinfection (pre-filtration) and post–granular activated carbon filtration.
With chlorine dioxide, Medema et al. (1991) reported CT99 values of 0.04–0.14 mg·min/L
for a drinking water strain of A. hydrophila. In the same study, a naturally occurring Aeromonas
population (predominantly A. sobria) was observed to be slightly more sensitive, with a reported
CT99 of 0.1 mg·min/L.
For UV disinfection, data produced by the U.S. EPA (2002) suggested the capability for a
1 and 2 log inactivation of A. hydrophila at doses of 3 and 8 mWs/cm2, respectively (equivalent
to 3 and 8 mJ/cm2)—doses significantly less than those commonly employed in water treatment.
In the distribution system, maintaining an adequate disinfectant residual should provide
control of Aeromonas in the finished water. The potential exists for Aeromonas to regrow in the
distribution system, however. During a year-long survey of a major drinking water distribution
system in Scotland, Gavriel et al. (1998) reported that although Aeromonas was not detected in
water samples collected downstream from chlorination prior to the distribution network, it could
occasionally be recovered from distribution samples, even at locations maintaining a substantial
chlorine residual (> 0.2 mg/L). Similarly, other studies have demonstrated that Aeromonas could
be detected in municipal distribution systems at locations having temperatures below 14°C and
chlorine residuals above 0.2 mg/L (Chauret et al., 2001; Pablos et al., 2009).
Elimination of Aeromonas in the distribution system once the organisms become
established in biofilms can be difficult (Holmes and Nicolls, 1995; Gavriel et al., 1998;
Långmark et al., 2007). Aeromonads sequestered in biofilms resist disinfection and persist for
long periods (U.S. EPA, 2006). Elements important for helping to control Aeromonas growth
include limiting the number of organisms entering the distribution system through effective
treatment, maintaining low water temperatures, providing appropriate free chlorine residuals,
limiting the levels of organic carbon compounds and proper maintenance of the distribution
system (WHO, 2010).
B.2.3.4 Assessment
Some studies have been undertaken to determine whether the indicators currently used in
the drinking water industry, including E. coli, total coliforms and HPC, can be used as surrogates
for the presence of Aeromonas. Several studies have showed no evidence of a relationship
between Aeromonas incidence and coliforms, E. coli or HPC (Holmes et al., 1996; Gavriel et al.,
1998; Fernández et al., 2000; Pablos et al., 2009). Although no direct correlation exists between
Aeromonas populations and total HPC, the organisms do make up a portion of HPC bacteria
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found in water and are detected by HPC tests (Pablos et al., 2009). The Netherlands has
established drinking water standards for A. hydrophila, consisting of a median value (over a 1year period) of 20 CFU/100 mL in water leaving the treatment plant and a 90th percentile value
(over a 1-year period) of 200 CFU/100 mL in distribution system water (van der Kooij, 2003;
Pablos et al., 2009). These values have been based on an assessment of achievability and are
motivated by a precautionary approach, rather than on the public health significance of their
occurrence in drinking water (WHO, 2002).
Aeromonas is not considered to be an indicator of faecal contamination or treatment
failure (U.S. EPA, 2002). The organisms have been proposed as a possible supplemental
indicator of drinking water quality by relating to the presence of biofilm. Therefore, if there are
significant increases in Aeromonas concentrations in a drinking water supply, this indicates a
general deterioration of bacteriological quality.
When looking at the overall public health significance of A. hydrophila in drinking water,
further epidemiological studies are needed for a better understanding of the relationship between
Aeromonas illness and the presence of these organisms in drinking water. Based on the current
evidence, treated drinking water likely represents a very low risk. It has been proposed that in
comparison with other pathogens that can potentially be acquired through drinking water,
Aeromonas is at the low end of the scale in terms of relative risk (Rusin et al., 1997; Janda and
Abbott, 2010). Nevertheless, it is advisable to minimize Aeromonas levels in drinking water
supplies as much as is practical until its public health significance has been fully investigated.
B.2.4 Helicobacter pylori
Helicobacter pylori is a recognized human pathogen that can colonize the stomach. The
understanding of how this organism is spread is still quite limited; however, it is believed that
there are a few routes of transmission, including through drinking water (Percival and Thomas,
2009). The majority of people infected with H. pylori are asymptomatic, and they may live their
entire lives with the organism. However, more serious disorders, such as peptic ulcers or stomach
cancer, can develop in a small percentage of cases.
Helicobacter are Gram-negative, motile, small curved rods that are closely related to
Campylobacter. The organisms have two distinct forms, a spiral rod shape and a shorter coccoid
form, which is taken on under conditions of stress. To date, the coccoid form has been found to
be non-culturable. The genus Helicobacter contains at least 25 species, as determined by
deoxyribonucleic acid (DNA) sequencing, of which H. pylori is the species of relevance for the
water industry. Other Helicobacter species have been detected in humans that have been
associated with gastric illness; however, these are not considered to be as prevalent as H. pylori.
B.2.4.1 Sources and exposure
The primary reservoir identified for H. pylori is the human stomach (Dunn et al., 1997;
Brown, 2000). It has been suggested that some animals (i.e., cats, dogs, sheep, primate monkeys)
can be infected by H. pylori, but the consensus at present is that they do not play a significant
role as reservoirs in transmitting this organism to humans (Baele et al., 2009; Haesebrouck et al.,
2009). Although H. pylori has been cultured from human faeces, its isolation from water using
culture methods has not been successful to date (Percival and Thomas, 2009). It is believed that
the spiral culturable form rapidly transforms into a viable, non-culturable state (coccoid form) in
the water environment. This is thought to be a response to environmental stresses, including
changes in temperature, nutrient availability and osmolarity (Adams et al., 2003; Percival and
Thomas, 2009.
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Exact details on the transmission of H. pylori remain unclear (Bellack et al., 2006). Based
on epidemiological findings, a higher risk of H. pylori infection exists among persons of low
economic status living in crowded conditions or unhygienic environments (Brown, 2000; Gomes
and De Martinis, 2004). Transfer mechanisms that have been proposed include gastric–oral, oral–
oral and faecal–oral (Percival and Thomas, 2009). Overall, it is speculated that person-to-person
transfer is the most likely route of transmission (Brown, 2000). The fact that it has not yet been
possible to culture viable Helicobacter from the water environment has raised questions
regarding the possibility of waterborne transmission. Nevertheless, there has been significant
evidence provided in support of water as an important source of infection. Molecular techniques
(PCR, fluorescent in situ DNA hybridization) have been used to confirm the presence of H.
pylori in natural waters (Hegarty et al., 1999; Sasaki et al., 1999; Horiuchi et al., 2001; Benson et
al., 2004; Moreno et al., 2007). As well, in the laboratory, H. pylori has been shown to survive
for periods ranging from days up to weeks in sterile river water, stream water, saline solution and
distilled water at a wide variety of pH values and at temperatures ranging from 4°C to 25°C
(West et al., 1992; Shahamat et al., 1993; Adams et al., 2003; Azevedo et al., 2008). As with
Legionella and mycobacteria, evidence has been supplied that biofilms and free-living
waterborne amoebae may provide environmental niches where H. pylori can persist (Park et al.,
2001; Winiecka-Krusnell et al., 2002; Watson et al., 2004; Bragança et al., 2007).
Waterborne transmission has been suggested as an important source of infection in
developing countries (Bellack et al., 2006). Supporting evidence has come from epidemiological
studies showing that individuals consuming untreated or contaminated waters had a high risk of
infection (Klein et al., 1991; Goodman et al., 1996; McKeown et al., 1999; Herbarth et al., 2001;
Brown et al., 2002; Rolle-Kampczyk et al., 2004). There has been less evidence supporting the
importance of waterborne transmission in developed countries (Percival and Thomas, 2009)
owing to the difficulty in isolating H. pylori from drinking water with culturable methods. These
difficulties in isolating the bacteria are due to changes in morphology, growth and metabolism
when H. pylori is exposed to varying environments (Bode et al., 1993). However, the detection of
H. pylori in drinking water distribution systems using molecular techniques suggests that it can
still play an important role (Baker and Hegarty, 2001; Watson et al., 2004; Gião et al., 2008;
Percival and Thomas, 2009). Additional research is required to provide further insight into the
persistence, viability and associated risk of H. pylori in drinking water systems.
The infectious dose necessary for colonization of humans is not known. Results of
challenge studies suggest that it is less than 104 cells and related to stomach pH (Solnick et al.,
2001; Graham et al., 2004). However, given the high percentage of infected individuals among
the population and the evidence from cases of accidental infection (e.g., from laboratory work,
use of improperly maintained endoscopes), the dose could be much lower (Langenberg et al.,
1990; Matysiak-Budnik et al., 1995).
B.2.4.2 Health effects
Human infection with H. pylori leads to gastritis, or inflammation of the stomach lining
(Dunn et al., 1997; Kusters et al., 2006). The organism colonizes the human stomach, stimulating
the immune system and inflammatory cells, and it is this response that brings about gastritis. In
the majority of H. pylori infections, there are no obvious signs of disease (Kusters et al., 2006). It
has been well established that infections with H. pylori are generally acquired during childhood,
with a lower frequency of infection in adults (Ernst and Gold, 2000; Allaker et al., 2002).
Further, infection, once established, is considered to be lifelong unless treatment is pursued
(Blaser, 1992; Kusters et al., 2006). Helicobacter pylori is the primary cause of peptic ulcers
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(Kuipers et al., 1995). It has been estimated that 85–95% of ulcers are the result of infection with
this organism (Kuipers et al., 1995). Carriage of H. pylori has also been recognized as an
important risk factor for the development of gastric cancer (i.e., gastric lymphoma and
adenocarcinoma) (Dunn et al., 1997; Pinto-Santini and Salama, 2005). Broad estimates of the risk
of infected persons developing these advanced diseases have been put at 10–20% for peptic
ulcers and 1–2% for gastric cancer (Ernst and Gold, 2000; Kusters et al., 2006).
Infection with H. pylori is treatable (Scott et al., 1998; Vakil and Megraud, 2007), and
data from animal and human infection studies suggest that an H. pylori vaccine is possible
(Graham et al., 2004; Del Guidice et al., 2009). This area of research is currently being explored.
B.2.4.3 Treatment technology
Similar to other bacteria, a proportion of the H. pylori present in the source water will be
removed using physical methods, such as conventional filtration (i.e., coagulation, flocculation
and sedimentation). Helicobacter pylori is also susceptible to disinfectants commonly used in
drinking water treatment (e.g., chlorine, UV, ozone and monochloramine).
Literature regarding the disinfection of H. pylori is limited when compared with that
available for other waterborne bacterial pathogens. Investigations are difficult because the cells of
H. pylori become viable but non-culturable in the environment, and this form cannot be detected
easily by regular culture methods (Moreno et al., 2007). With chlorination, data provided from
the few reported studies suggest log reductions of culturable H. pylori cells ranging from 0.3 log
at a chlorine concentration of 0.1 mg/L for 1 minute (Baker et al., 2002) to > 4 log at a chlorine
concentration of 0.5 mg/L for 80 seconds (Johnson et al., 1997) to approximately 7 log at a
chlorine concentration of 1 mg/L for 5 minutes (Moreno et al., 2007). Moreno et al. (2007)
conducted research using a combination of direct viable count and fluorescent in situ DNA
hybridization methods specifically to study the effects of chlorination on H. pylori cell viability.
The researchers demonstrated that viable H. pylori cells could be detected after 3 hours of
exposure to a chlorine concentration of 1.0 mg/L, but not after 24 hours of exposure.
The current body of research suggests that the CT provided by a conventional water
treatment plant is sufficient to inactivate H. pylori in the finished water. However, if H. pylori
does enter the distribution system, potentially through a break in treatment or infiltration into the
system, disinfectant residuals maintained in the distribution system are probably insufficient for
inactivation (Baker et al., 2002). Disinfectant CT99 values for H. pylori reported by Baker et al.
(2002) were 0.24 mg/L min for ozone, 0.299 mg/L min for chlorine and 9.5 mg/L min for
monochloramine. In terms of response to disinfection, compared with E. coli, Baker et al. (2002)
reported that H. pylori was statistically more resistant to chlorine and ozone, but not to
monochloramine. Other authors have similarly reported H. pylori having greater resistance to
chlorine compared with E. coli (Johnson et al., 1997; Moreno et al., 2007). For UV disinfection,
Hayes et al. (2006) reported a greater than 4 log inactivation of culturable H. pylori cells at
fluences of less than 8 mJ/cm2.
Association with biofilms has also been shown to protect H. pylori from disinfectants,
similar to other bacterial pathogens. Gião et al. (2010) observed that H. pylori cells (measured by
peptide nucleic acid probe) remained viable for at least 26 days following exposure to chlorine at
0.2 and 1.2 mg/L. Also, in contrast to findings provided by other researchers, the authors
observed that H. pylori cells in suspension did not lose culturability after 30 minutes of exposure
to chlorine at an initial concentration of 1.2 mg/L (Gião et al., 2010). Successful distribution
system control of Helicobacter would similarly be aided by management steps to reduce the
formation of biofilm and the presence of free-living amoebae in this environment.
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B.2.4.4 Assessment
Overall, the predominant transmission route for H. pylori seems to be situation dependent,
with person-to-person transmission playing a key role in many circumstances. Water and food
appear to be of lesser direct importance, but they can still play a significant role in situations with
improper sanitation and lax hygiene
Much is still unknown regarding the ecology and behaviour of H. pylori in water systems.
However, sufficient information has been provided to suggest that H. pylori can be regarded as a
potential human pathogen with the potential for waterborne transmission. Illness associated with
H. pylori infection is of a mild or benign nature in the majority of cases, and outbreaks of illness
have not been linked to the presence of H. pylori in drinking water supplies. Further research is
needed to provide clarity on such topics as its presence in source waters, its susceptibility to
treatment and disinfection, and its overall significance for drinking water systems in Canada.
B.3
Issues of emerging interest
B.3.1 Disinfection and antibiotic-resistant organisms
Disinfectants and antibiotics exert action on bacteria through very different mechanisms.
Antibiotics characteristically act against specific target sites within the bacteria, interfering with a
particular component of an essential process or pathway. In contrast, disinfectants act in a general
manner against multiple targets that are fundamental components of the bacterial cell (e.g.,
proteins and DNA/ribonucleic acid [RNA]). Free chlorine, chloramine, chlorine dioxide and
ozone are all very strong oxidizers ,which inactivate bacterial cells by destroying the activity of
cell proteins that can be involved with cell structure or metabolism. UV light inactivates bacterial
cells by altering the DNA in such a way that the cell can no longer multiply. Because of the
fundamental differences in the way in which these two types of antibacterial strategies operate,
antibiotic-resistant bacteria are not expected to show increased resistance to the action of drinking
water disinfectants.
Antibiotic-resistant pathogens have the ability to change and become less susceptible to
drugs. Bacterial resistance to antibiotics can be brought about in a variety of ways; for example,
cells may not allow penetration of the antibiotic, they may lack the required target site or they
may possess enzymes that can modify or destroy the antibiotic. Repeated exposure of bacteria to
antibacterial agents and access of bacteria to increasingly large pools of antibiotic-resistant genes
in mixed bacterial populations are the primary driving forces for emerging antibacterial
resistance.
There are numerous types of antibiotics, which can be categorized into different classes
based on their structure or mode of action. Bacteria having a particular resistance mechanism
may be unaffected by antibiotics of a similar class or that target the same site. These same
bacteria may be vulnerable to different antibiotics or may possess mechanisms that make them
resistant to multiple classes of antibiotics. The growing problem with antibacterial resistance is
diminution of the effectiveness of antibacterial agents, resulting in antibiotic-resistant pathogens
that are more virulent than their susceptible counterparts, causing more prolonged or severe
illnesses.
Very few data have been generated to date regarding the effects of disinfectants on
antibiotic-resistant bacteria in drinking water. Some early work found that a greater proportion of
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HPC bacteria in treated water are antibiotic-resistant bacteria, compared with those in untreated
water (Armstrong et al., 1981, 1982). Templeton et al. (2009) conducted an investigation on the
susceptibility of ampicillin- and trimethoprim-resistant strains of E. coli to free chlorine and UV
disinfection. The authors observed no differences in UV inactivation between antibiotic-resistant
and antibiotic-sensitive E. coli under the doses and contact times tested. The trimethoprimresistant E. coli strain did show slightly greater resistance to free chlorine compared with the
antibiotic-sensitive E. coli; however, the authors concluded that the difference was likely to be
negligible under chlorine doses and contact times typically observed in routine drinking water
treatment. It was further concluded that these disinfectants did not likely select for ampicillin or
trimethoprim resistance during drinking water treatment. No drinking water studies were found
pertaining to the inactivation rates for other disinfectants, such as ozone or chlorine dioxide,
against antibiotic-resistant bacteria.
At present, there is little evidence to indicate that the use of disinfectants in drinking
water systems favours the selection of antibiotic-resistant bacteria in any way (Templeton et al.,
2009). However, one study by Xi et al. (2009) suggested that water treatment could increase the
antibiotic resistance of surviving bacteria or induce antibiotic resistance gene transfer. Additional
study in this area is needed. The evidence at present, although limited, suggests that antibiotic
resistance in bacteria is not an important factor in chlorine and UV treatment effectiveness at
doses and contact times typically applied in drinking water treatment systems.
B.3.2 Showerheads
Shower use can provide a source of exposure to microorganisms through aerosolization,
as the inside of a showerhead provides a moist, warm, dark environment that is frequently
replenished with low-level nutrient sources.
Inhalation of aerosols from showerhead water has been implicated in respiratory disease
(Falkinham et al., 2008; Feazel et al., 2009). Although opportunistic pathogens have been
cultured from showerheads, little is known about either the prevalence or the nature of the
microorganisms that can be aerosolized during showering. To determine the composition of
showerhead biofilms and waters, Feazel et al. (2009) analysed ribosomal RNA gene sequences of
biofilms from 45 showerheads from nine sites in the United States. The authors found that
sequences representative of non-tuberculous mycobacteria and other opportunistic pathogens
were highly enriched in many showerhead biofilms. They concluded that showerheads may
present a significant potential exposure to aerosolized microorganisms and that the health risk
associated with showerheads needs further investigation, particularly for individuals with
compromised immune or respiratory systems.
B.4
Residential-scale treatment
B.4.1 Residential-scale and private drinking water systems
Residential-scale2 treatment is also applicable to small drinking water systems. This
would include both privately owned systems and systems with a minimal or no distribution
2
For the purposes of this document, a residential-scale water supply system is defined as a system, with a minimal or
no distribution system, that provides water to the public from a facility not connected to a municipal supply.
Examples of such facilities include schools, personal care homes, day care centres, hospitals, community wells,
hotels and restaurants. The definition of a residential-scale supply may vary between jurisdictions.
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system that provide water to the public from a facility not connected to a municipal supply
(previously referred to as semi-public systems).
The presence of E. coli in a residential-scale or private drinking water system indicates
that the source or the system has likely been affected by recent faecal contamination; as a result,
the water should be deemed as unsafe to drink. The absence of E. coli during routine verification
should be an adequate indication of the sufficient removal and inactivation of enteric bacterial
pathogens. Where applicable, testing frequencies for residential-scale systems will be determined
by the responsible authority and should include times when the risk of contamination is
greatest—for example, in early spring after the thaw, after an extended dry spell or following
heavy rains. For owners of private supplies, existing wells should be tested two to three times per
year and during these same periods. New or rehabilitated wells should also be tested before use to
confirm microbiological safety.
Non-faecal bacterial pathogens that occur naturally in the water environment can be found
in groundwater, although typically at a lower frequency and in lower numbers than in surface
waters. The levels of organisms necessary to cause disease in healthy individuals are uncertain,
although limited study has suggested that reasonably elevated numbers beyond those typically
found in source waters are required. These organisms are most likely to be found in distribution
system biofilms and can survive and grow there to reach significant populations. In smaller
systems, distribution system biofilms are less of a concern than in municipal systems, because
distribution systems are smaller or non-existent and the retention time for the finished water is
shorter.
Various options are available for treating source waters to provide high-quality pathogenfree drinking water. These include filtration and disinfection with chlorine-based compounds or
alternative technologies, such as UV light. These technologies are similar to the municipal
treatment barriers, but on a smaller scale.
Private homeowners should also be aware that domestic hot water systems can be
contaminated with Legionella; as a result, water heaters should be kept at a suitable temperature
(at least 60ºC) to protect against the potential growth of this organism. The National Plumbing
Code of Canada includes requirements for a minimum water temperature of 60°C in hot water
storage tanks to address the growth of Legionella (NRCC, 2010). Homeowners should also take
appropriate safety measures to reduce the risk of scalding at the tap. These measures include
installing thermostatic or pressure-balanced mixing valves to control the water temperature at the
tap (Bartram et al., 2007; Bentham et al., 2007). This strategy may also be useful in reducing
other microorganisms in hot water heaters, as many of them do not survive at this higher
temperature (LeChevallier and Au, 2004; AWWA, 2006).
Larger plumbing systems could use additional control measures. These measures include
temperature control; control of water system design and construction to prevent the accumulation
of biofilms, sediments or deposits; and nutrient control strategies (Bartram et al., 2007; Bentham
et al., 2007).
B.4.2 Use of residential-scale treatment devices
The information on treatment, disinfection and inactivation of microorganisms in this
document is relevant primarily to municipal-scale systems. Municipal treatment of drinking water
is designed to reduce microbial contaminants to levels below those typically shown to be
associated with disease. The use of residential-scale treatment devices on municipally treated
water is generally not necessary, but is primarily based on individual choice. In cases where small
systems or individual households obtain drinking water from private wells or surface water
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supplies such as lakes, treatment devices can be used as an additional barrier for reducing
pathogen concentrations in drinking water.
Health Canada does not recommend specific brands of drinking water treatment devices,
but it strongly recommends that consumers use devices that have been certified by an accredited
certification body as meeting the appropriate NSF International/American National Standards
Institute drinking water treatment unit standards. These standards have been designed to
safeguard drinking water by helping to ensure the material safety and performance of products
that come into contact with drinking water. Certification organizations provide assurance that a
product conforms to applicable standards and must be accredited by the Standards Council of
Canada.
Point-of-use systems (installed at the faucet) and point-of-entry systems (installed where
water enters the home) are of interest for use in treatment and disinfection of drinking water in
small, rural or remote communities, particularly those using a groundwater source. The most
common types of treatment device that are generally able to inactivate waterborne pathogens
(including bacteria) use UV disinfection. Although membrane filtration (reverse osmosis) may be
able to reduce pathogens, certified devices are generally intended for use on water supplies
deemed microbiologically safe. Before a treatment device is installed, the water should be tested
to determine its general water chemistry. Periodic testing by an accredited laboratory should be
conducted on both the water entering the treatment device and the finished water to verify that
the treatment device is effective. Devices can lose removal capacity through usage and time and
need to be maintained and/or replaced. Consumers should verify the expected longevity of the
components (e.g., UV lamp, membrane) in their treatment device as per the manufacturer’s
recommendations and service the device when required. Homeowners should ensure that the
selection and installation of treatment devices comply with applicable local regulations.
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Part C. References and acronyms
C.1
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C.2
AIDS
CFU
CT
DAEC
DNA
EAEC
EHEC
EIEC
EPA
EPEC
ETEC
HIV
HPC
Mac
PCR
RNA
UV
List of acronyms
acquired immunodeficiency syndrome
colony-forming unit
concentration × time
diffuse adherent E. coli
deoxyribonucleic acid
enteroaggregative E. coli
enterohaemorrhagic E. coli
enteroinvasive E. coli
Environmental Protection Agency (U.S.)
enteropathogenic E. coli
enterotoxigenic E. coli
human immunodeficiency virus
heterotrophic plate count
Mycobacterium avium complex
polymerase chain reaction
ribonucleic acid
ultraviolet
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February 2013
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