Pathogenic E. coli© 2008 Kenneth Todar University of Wisconsin-Madison Department of Bacteriology E. coli O157:H7. Phase contrast image of cells immobilized on an agar-coated slide. William Ghiorse, Department of Microbiology, Cornell University, Ithaca, New York. Licensed for use by ASM Microbe Library http://www.microbelibrary.org.
Theodor Escherich first described E. coli in 1885, as Bacterium coli commune, which he isolated from the feces of newborns. It was later renamed Escherichia coli, and for many years the bacterium was simply considered to be a commensal organism of the large intestine. It was not until 1935 that a strain of E. coli was shown to be the cause of an outbreak of diarrhea among infants.
The GI tract of most warm-blooded animals is colonized by E. coli
within hours or a few days after birth. The bacterium is ingested in foods or water or obtained directly from other individuals handling the infant. The human bowel is usually colonized within 40 hours of birth. E. coli
can adhere to the mucus overlying the large intestine. Once established, an E. coli
strain may persist for months or years. Resident strains shift over a long period (weeks to months), and more rapidly after enteric infection or antimicrobial chemotherapy that perturbs the normal flora. The basis for these shifts and the ecology of Escherichia coli
in the intestine of humans are poorly understood despite the vast amount of information on almost every other aspect of the organism's existence. The entire DNA base sequence of the E. coli
genome has been known since 1997.
E. coli is the head of the large bacterial family, Enterobacteriaceae, the enteric bacteria, which are facultatively anaerobic Gram-negative rods that live in the intestinal tracts of animals in health and disease. The Enterobacteriaceae are among the most important bacteria medically. A number of genera within the family are human intestinal pathogens (e.g. Salmonella, Shigella, Yersinia). Several others are normal colonists of the human gastrointestinal tract (e.g. Escherichia, Enterobacter, Klebsiella), but these bacteria, as well, may occasionally be associated with diseases of humans.
Physiologically, E. coli is versatile and well-adapted to its characteristic habitats. It can grow in media with glucose as the sole organic constituent. Wild-type E. coli has no growth factor requirements, and metabolically it can transform glucose into all of the macromolecular components that make up the cell. The bacterium can grow in the presence or absence of O2. Under anaerobic conditions it will grow by means of fermentation, producing characteristic "mixed acids and gas" as end products. However, it can also grow by means of anaerobic respiration, since it is able to utilize NO3, NO2 or fumarate as final electron acceptors for respiratory electron transport processes. In part, this adapts E. coli to its intestinal (anaerobic) and its extraintestinal (aerobic or anaerobic) habitats.
E. coli can respond to environmental signals such as chemicals, pH, temperature, osmolarity, etc., in a number of very remarkable ways considering it is a unicellular organism. For example, it can sense the presence or absence of chemicals and gases in its environment and swim towards or away from them. Or it can stop swimming and grow fimbriae that will specifically attach it to a cell or surface receptor. In response to change in temperature and osmolarity, it can vary the pore diameter of its outer membrane porins to accommodate larger molecules (nutrients) or to exclude inhibitory substances. With its complex mechanisms for regulation of metabolism the bacterium can survey the chemical contents in its environment in advance of synthesizing any enzymes that metabolize these compounds. It does not wastefully produce enzymes for degradation of carbon sources unless they are available, and it does not produce enzymes for synthesis of metabolites if they are available as nutrients in the environment.
E. coli is a consistent inhabitant of the human intestinal tract, and it is the predominant facultative organism in the human GI tract; however, it makes up a very small proportion of the total bacterial content. The anaerobic Bacteroides species in the bowel outnumber E. coli by at least 20:1. however, the regular presence of E. coli in the human intestine and feces has led to tracking the bacterium in nature as an indicator of fecal pollution and water contamination. As such, it is taken to mean that, wherever E. coli is found, there may be fecal contamination by intestinal parasites of humans.
Unstained cells of E. coli viewed by phase microscopy. about 1000X magnification. CDC.
Escherichia coli in the Gastrointestinal Tract
The commensal E. coli strains that inhabit the large intestine of all humans and warm-blooded animals comprise no more than 1% of the total bacterial biomass.
The E. coli flora is apparently in constant flux. One study on the distribution of different E. coli strains colonizing the large intestine of women during a one year period (in a hospital setting) showed that 52.1% yielded one serotype, 34.9% yielded two, 4.4% yielded three, and 0.6% yielded four. The most likely source of new serotypes of E. coli is acquisition by the oral route.
To study oral acquisition, the carriage rate of E. coli carrying antibiotic-resistance plasmids (R factors) was examined among vegetarians, babies, and nonvegetarians. It was assumed that nonvegetarians might carry more E. coli with R factors due to their presumed high incidence in animals treated with growth-promoting antimicrobial agents. However, omnivores had no higher an incidence of R-factor-containing E. coli than vegetarians, and babies had more resistant E. coli in their feces than nonvegetarians. No suitable explanation could be offered for these findings. Besides, investigation of the microbial flora of the uninhabited Krakatoa archipelago has shown the presence of antibiotic-resistant E. coli associated with plants.
The bottom line seems to be that most of us have more than one strain of E. coli in our gut, and intestinal strains tend to displace one another about three or four times a year.
Pathogenesis of E. coli
Over 700 antigenic types (serotypes
) of E. coli
are recognized based on O, H, and K antigens
. At one time serotyping was important in distinguishing the small number of strains that actually cause disease. Thus, the serotype O157:H7 (O refers to somatic antigen; H refers to flagellar antigen) is uniquely responsible for causing HUS (hemolytic uremic syndrome). Nowadays, particularly for diarrheagenic strains (those that cause diarrhea) pathogenic E. coli
are classified based on their unique virulence factors and can only be identified by these traits. Hence, analysis for pathogenic E. coli
usually requires that the isolates first be identified as E. coli
before testing for virulence markers.
Pathogenic strains of E. coli
are responsible for three types of infections in humans: urinary tract infections (UTI)
, neonatal meningitis
, and intestinal diseases (gastroenteritis)
. The diseases caused (or not caused) by a particular strain of E. coli
depend on distribution and expression of an array of virulence determinants, including adhesins, invasins, toxins, and abilities to withstand host defenses. These are summarized in Table 1 and applied to the discussion of pathogenic strains E. coli
Table 1. Summary of the Virulence Determinants of Pathogenic E. coli
Type 1 fimbriae
Intimin (non-fimbrial adhesin)
EPEC adherence factor
Shigella-like "invasins" for intracellular invasion and spread
Antiphagocytic surface properties
Defense against serum bactericidal reactions
Defense against immune responses
genetic exchange by transduction and conjugation
R factors and drug resistance plasmids
toxin and other virulence plasmids
siderophores and siderophore uptake systems
Urinary Tract InfectionsUropathogenic E. coli (UPEC)
cause 90% of the urinary tract infections (UTI) in anatomically-normal, unobstructed urinary tracts. The bacteria colonize from the feces or perineal region and ascend the urinary tract to the bladder. Bladder infections are 14-times more common in females than males by virtue of the shortened urethra. The typical patient with uncomplicated cystitis is a sexually-active female who was first colonized in the intestine with a uropathogenic E. coli
strain. The organisms are propelled into the bladder from the periurethral region during sexual intercourse. With the aid of specific adhesins they are able to colonize the bladder.
The adhesin that has been most closely associated with uropathogenic E. coli is the P fimbria (or pyelonephritis-associated pili [PAP]). The letter designation is derived from the ability of P fimbriae to bind specifically to the P blood group antigen which contains a D-galactose-D-galactose residue. The fimbriae bind not only to red cells but to a specific galactose dissaccharide that is found on the surfaces uroepithelial cells in approximately 99% of the population.
The frequency of the distribution of this host cell receptor plays a role in susceptibility and explains why certain individuals have repeated UTI caused by E. coli. Uncomplicated E. coli UTI virtually never occurs in individuals lacking the receptors.
Uropathogenic strains of E. coli possess other determinants of virulence in addition to P fimbriae. E. coli with P fimbriae also possess the gene for Type 1 fimbriae, and there is evidence that P fimbriae are derived from Type 1 fimbriae by insertion of a new fimbrial tip protein to replace the mannose-binding domain of Type 1 fimbriae. In any case, Type 1 fimbriae could provide a supplementary mechanism of adherence or play a role in aggregating the bacteria to a specific manosyl-glycoprotein that occurs in urine.
Uropathogenic strains of E. coli usually produce siderophores that probably play an essential role in iron acquisition for the bacteria during or after colonization. They also produce hemolysins which are cytotoxic due to formation of transmembranous pores in host cell membranes. One strategy for obtaining iron and other nutrients for bacterial growth may involve the lysis of host cells to release these substances. The activity of hemolysins is not limited to red cells since the alpha-hemolysins of E. coli also lyse lymphocytes, and the beta-hemolysins inhibit phagocytosis and chemotaxis of neutrophils.
Another factor thought to be involved in the pathogenicity of the uropathogenic strains of E. coli is their resistance to the complement-dependent bactericidal effect of serum. The presence of K antigens is associated with upper urinary tract infections, and antibody to the K antigen has been shown to afford some degree of protection in experimental infections. The K antigens of E. coli are "capsular" antigens that may be composed of proteinaceous organelles associated with colonization (e.g., CFA antigens), or made of polysaccharides. Regardless of their chemistry, these capsules may be able to promote bacterial virulence by decreasing the ability of antibodies and/or complement to bind to the bacterial surface, and the ability of phagocytes to recognize and engulf the bacterial cells. The best studied K antigen, K-1, is composed of a polymer of N-acetyl neuraminic acid (sialic acid), which besides being antiphagocytic, has the additional property of being an antigenic disguise.
Neonatal MeningitisNeonatal meningitis
affects 1/2,000-4,000 infants. Eighty percent of E. coli
strains involved synthesize K-1 capsular antigens (K-1 is only present 20-40% of the time in intestinal isolates).
E. coli strains invade the blood stream of infants from the nasopharynx or GI tract and are carried to the meninges.
The K-1 antigen is considered the major determinant of virulence among strains of E. coli that cause neonatal meningitis. K-1 is a homopolymer of sialic acid. It inhibits phagocytosis, complement, and responses from the host's immunological mechanisms. K-1 may not be the only determinant of virulence, however, as siderophore production and endotoxin are also likely to be involved.
Epidemiologic studies have shown that pregnancy is associated with increased rates of colonization by K-1 strains and that these strains become involved in the subsequent cases of meningitis in the newborn. Probably, the infant GI tract is the portal of entry into the bloodstream. Fortunately, although colonization is fairly common, invasion and the catastrophic sequelae are rare.
Neonatal meningitis requires antibiotic therapy that usually includes ampicillin and a third-generation cephalosporin.
Lysis of a dividing pair of E. coli cells in the presence of a beta-lactam antibiotic. Some beta lactam antibiotics, such as ampicillin and cephalosporin, are effective in the treatment of meningitis caused by strains of E. coli (above). The beta lactam antibiotics prevent cell wall synthesis and assembly in the bacterium. When the bacterium grows in the presence of the antibiotic, the cell wall becomes progressively weaker and weaker, so the the organism eventually ruptures or "lyses", pouring out its cytoplasmic contents as shown here.
Intestinal Diseases Caused by E. coli
As a pathogen, E. coli
is best known for its ability to cause intestinal diseases. Five classes (virotypes) of E. coli
that cause diarrheal diseases are now recognized: enterotoxigenic E. coli (ETEC), enteroinvasive E. coli (EIEC), enterohemorrhagic E. coli (EHEC), enteropathogenic E. coli (EPEC), and enteroaggregative E. coli (EAEC)
. Each class falls within a serological subgroup and manifests distinct features in pathogenesis. A summary of the characteristics of diarrheagenic strains of E. coli
is given in Table 2 at the end of this article.Enterotoxigenic E. coli (ETEC)
is an important cause of diarrhea in infants and travelers in underdeveloped countries or regions of poor sanitation. In the U.S., it has been implicated in sporadic waterborne outbreaks, as well as due to the consumption of soft cheeses, Mexican-style foods and raw vegetables. The diseases vary from minor discomfort to a severe cholera-like syndrome. ETEC are acquired by ingestion of contaminated food and water, and adults in endemic areas evidently develop immunity. The disease requires colonization and elaboration of one or more enterotoxins. Both traits are plasmid-encoded.
ETEC may produce a heat-labile enterotoxin (LT)
that is similar in molecular size, sequence, antigenicity, and function to the cholera toxin (Ctx). It is an 86kDa protein composed of an enzymatically active (A) subunit surrounded by 5 identical binding (B) subunits. It binds to the same identical ganglioside receptors that are recognized by the cholera toxin (i.e., GM1), and its enzymatic activity is identical to that of the cholera toxin.
ETEC may also produce a heat stable toxin (ST)
that is of low molecular size and resistant to boiling for 30 minutes. There are several variants of ST, of which ST1a or STp is found in E. coli
isolated from both humans and animals, while ST1b or STh is predominant in human isolates only. The ST enterotoxins are peptides of molecular weight about 4,000 daltons. Their small size explains why they are not inactivated by heat. ST causes an increase in cyclic GMP in host cell cytoplasm leading to the same effects as an increase in cAMP. ST1a is known to act by binding to a guanylate cyclase that is located on the apical membranes of host cells, thereby activating the enzyme. This leads to secretion of fluid and electrolytes resulting in diarrhea.
The infective dose of ETEC for adults has been estimated to be at least 108
cells; but the young, the elderly and the infirm may be susceptible to lower numbers.
ETEC adhesins are fimbriae which are species-specific. For example, the K-88 fimbrial Ag is found on strains from piglets; K-99 Ag is found on strains from calves and lambs; CFA I, and CFA II, are found on strains from humans. These fimbrial adhesins adhere to specific receptors on enterocytes of the proximal small intestine.
Symptoms ETEC infections include diarrhea without fever
. The bacteria colonize the GI tract by means of a fimbrial adhesin, e.g. CFA I and CFA II, and are noninvasive
, but produce either the LT or ST toxin. <>Enteroinvasive E. coli (EIEC)
closely resemble Shigella
in their pathogenic mechanisms and the kind of clinical illness they produce. EIEC penetrate and multiply within epithelial cells of the colon causing widespread cell destruction. The clinical syndrome is identical to Shigella
dysentery and includes a dysentery-like diarrhea with fever
. EIEC apparently lack fimbrial adhesins but do possess a specific adhesin that, as in Shigella
, is thought to be an outer membrane protein. Also, like Shigella
, EIEC are invasive
organisms. They do not produce LT or ST toxin.
There are no known animal reservoirs of EIEC. Hence the primary source for EIEC appears to be infected humans. Although the infective dose of Shigella
is low (in the range of 10 to few hundred cells), volunteer feeding studies showed that at least 106
EIEC organisms are required to cause illness in healthy adults. Unlike typical E. coli
, EIEC are non-motile, do not decarboxylate lysine and do not ferment lactose. Pathogenicity of EIEC is primarily due to its ability to invade and destroy colonic tissue. The invasion phenotype, encoded by a high molecular weight plasmid, can be detected by PCR and probes for specific for invasion genes.Enteropathogenic E. coli (EPEC)
EPEC induce a profuse watery, sometimes bloody, diarrhea
. They are a leading cause of infantile diarrhea in developing countries. Outbreaks have been linked to the consumption of contaminated drinking water as well as some meat products. Pathogenesis of EPEC involves
a plasmid-encoded protein referred to as EPEC adherence factor
) that enables localized adherence of bacteria to intestinal cells and a non fimbrial adhesin designated intimin
, which is an outer membrane protein that mediates the final stages of adherence. They do not produce ST or LT toxins.
Adherence of EPEC strains to the intestinal mucosa is a very complicated process and produces dramatic effects in the ultrastructure of the cells resulting in rearrangements of actin in the vicinity of adherent bacteria. The phenomenon is sometimes called "attachment and effacing" of cells. EPEC strains are said to be "moderately-invasive", meaning they are not as invasive as Shigella, and unlike ETEC or EAEC, they cause an inflammatory response. The diarrhea and other symptoms of EPEC infections probably are caused by bacterial invasion of host cells and interference with normal cellular signal transduction, rather than by production of toxins.Enteroaggregative E. coli (EAEC)
Through volunteer feeding studies the infectious dose of EPEC in healthy adults has been estimated to be 106 organisms.
Some types of EPEC are referred to as diffusely adherent E. coli (DAEC), based on specific patterns of adherence. They are an important cause of traveler's diarrhea in Mexico and in North Africa.
The distinguishing feature of EAEC
strains is their ability to attach to tissue culture cells in an aggregative manner. These strains are associated with persistent diarrhea in young children. They resemble ETEC strains in that the bacteria adhere to the intestinal mucosa and cause non-bloody diarrhea without invading or causing inflammation. This suggests that the organisms produce an enterotoxin of some sort. Recently, a distinctive heat-labile plasmid-encoded toxin has been isolated from these strains, called the EAST
. They also produce a hemolysin
related to the hemolysin produced by E. coli
strains involved in urinary tract infections. The role of the toxin and the hemolysin in virulence has not been proven. The significance of EAEC strains in human disease is controversial. Enterohemorrhagic E. coli (EHEC)
are recognized as the primary cause of hemorrhagic colitis (HC)
or bloody diarrhea, which can progress to the potentially fatal hemolytic uremic syndrome (HUS)
. EHEC are characterized by the production of verotoxin or Shiga toxins
(Stx). Although Stx1 and Stx2 are most often implicated in human illness, several variants of Stx2 exist.
There are many serotypes of Stx-producing E. coli
, but only those that have been clinically associated with HC are designated as EHEC. Of these, O157:H7
is the prototypic EHEC and most often implicated in illness worldwide. The infectious dose for O157:H7 is estimated to be 10 - 100 cells; but no information is available for other EHEC serotypes. EHEC infections are mostly food or water borne and have implicated undercooked ground beef, raw milk, cold sandwiches, water, unpasteurized apple juice and vegetables
EHEC are considered to be "moderately invasive". Nothing is known about the colonization antigens of EHEC but fimbriae are presumed to be involved. The bacteria do not invade mucosal cells as readily as Shigella, but EHEC strains produce a toxin that is virtually identical to the Shiga toxin. The toxin plays a role in the intense inflammatory response produced by EHEC strains and may explain the ability of EHEC strains to cause HUS. The toxin is phage encoded and its production is enhanced by iron deficiency.
E. coli O157:H7 Transmission EM. American Society for Microbiology
Table 2. Diarrheagenic E. coli: virulence determinants and characteristics of disease
fimbrial adhesins e.g. CFA I, CFAII, K88. K99
produce LT and/or ST toxin
watery diarrhea in infants and travelers; no inflammation, no fever
nonfimbrial adhesins, possibly outer membrane protein
invasive (penetrate and multiply within epithelial cells)
does not produce shiga toxin
dysentery-like diarrhea (mucous, blood), severe inflammation, fever EPEC
non fimbrial adhesin (intimin)
EPEC adherence factor (EAF) enables localized adherence of bacteria to intestinal cells
moderately invasive (not as invasive as Shigella
does not produce LT or ST; some reports of shiga-like toxin
usually infantile diarrhea; watery diarrhea with blood, some inflammation, no fever; symptoms probably result mainly from invasion rather than toxigenesis EAEC
adhesins not characterized
produce ST-like toxin (EAST) and a hemolysin
persistent diarrhea in young children without inflammation or fever EHEC
adhesins not characterized, probably fimbriae
does not produce LT or ST but does produce shiga toxin
pediatric diarrhea, copious bloody discharge (hemorrhagic colitis), intense inflammatory response, may be complicated by hemolytic uremia
What is E. coli and where does it come from?
E. coli is a type of fecal coliform bacteria commonly found in the intestines of animals and humans. E. coli is short for Escherichia coli. The presence of E. coli in water is a strong indication of recent sewage or animal waste contamination. Sewage may contain many types of disease-causing organisms.
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What are fecal coliforms?
Fecal coliforms are bacteria that are associated with human or animal wastes. They usually live in human or animal intestinal tracts, and their presence in drinking water is a strong indication of recent sewage or animal waste contamination.
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How does E. coli or other fecal coliforms get in the water?
E. coli comes from human and animal wastes. During rainfalls, snow melts, or other types of precipitation, E. coli may be washed into creeks, rivers, streams, lakes, or ground water. When these waters are used as sources of drinking water and the water is not treated or inadequately treated, E. coli may end up in drinking water.
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What are the health effects of E. coli O157:H7?
E. coli O157:H7 is one of hundreds of strains of the bacterium E. coli. Although most strains are harmless and live in the intestines of healthy humans and animals, this strain produces a powerful toxin and can cause severe illness. Infection often causes severe bloody diarrhea and abdominal cramps; sometimes the infection causes non-bloody diarrhea. Frequently, no fever is present. It should be noted that these symptoms are common to a variety of diseases, and may be caused by sources other than contaminated drinking water.
In some people, particularly children under 5 years of age and the elderly, the infection can also cause a complication called hemolytic uremic syndrome, in which the red blood cells are destroyed and the kidneys fail. About 2%-7% of infections lead to this complication. In the United States, hemolytic uremic syndrome is the principal cause of acute kidney failure in children, and most cases of hemolytic uremic syndrome are caused by E. coli O157:H7. Hemolytic uremic syndrome is a life-threatening condition usually treated in an intensive care unit. Blood transfusions and kidney dialysis are often required. With intensive care, the death rate for hemolytic uremic syndrome is 3%-5%.
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How long does it take for these symptoms of E. coli O157:H7 infection to occur?
Symptoms usually appear within 2 to 4 days, but can take up to 8 days. Most people recover without antibiotics or other specific treatment in 5-10 days. There is no evidence that antibiotics improve the course of disease, and it is thought that treatment with some antibiotics may precipitate kidney complications. Antidiarrheal agents, such as loperamide (Imodium), should also be avoided.
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What should I do if I have any of the above symptoms?
Consult with your physician. Infection with E. coli O157:H7 is diagnosed by detecting the bacterium in the stool. Most laboratories that culture stool do not test for E. coli O157:H7, so it is important to request that the stool specimen be tested on sorbitol-MacConkey (SMAC) agar for this organism. All persons who suddenly have diarrhea with blood should get their stool tested for E. coli O157:H7.
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Are there groups of people who are at greater risk of getting any of the symptoms?
Children under the age of five, the elderly, and people whose health is immunocompromised (i.e., people who have long-term illnesses such as cancer or AIDS) are at greater risk of severe illness.
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What should these people who are at greater risk do? Are there any additional precautions they should take?
People who are at greater risk should consult with their doctor or health care provider and follow the instructions provided.
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How will I know if my water is safe?
If you get your water from a public water system, then your water system is required by law to notify you if your water is not safe. If you are interested in obtaining information about your drinking water, consult the water quality report that you should receive annually from your local water system, or call your local water system directly.
Information on local water systems is also available on EPA's web site.
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How is water treated to protect me from E. coli?
The water can be treated using chlorine, ultra-violet light, or ozone, all of which act to kill or inactivate E. coli. Systems using surface water sources are required to disinfect to ensure that all bacterial contamination is inactivated, such as E. coli.
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How does the U.S. Environmental Protection Agency regulate E. coli?
According to EPA regulations, a system that operates at least 60 days per year, and serves 25 people or more or has 15 or more service connections, is regulated as a public water system under the Safe Drinking Water Act. If a system is not a public water system as defined by EPA's regulations, it is not regulated under the Safe Drinking Water Act, although it may be regulated by state or local authorities.
Under the Safe Drinking Water Act, EPA requires public water systems to monitor for coliform bacteria. Systems analyze first for total coliform, because this test is faster to produce results. Any time that a sample is positive for total coliform, the same sample must be analyzed for either fecal coliform or E. coli. Both are indicators of contamination with animal waste or human sewage.
The largest public water systems (serving millions of people) must take at least 480 samples per month. Smaller systems must take at least five samples a month unless the state has conducted a sanitary survey – a survey in which a state inspector examines system components and ensures they will protect public health – at the system within the last five years.
Systems serving 25 to 1,000 people typically take one sample per month. Some states reduce this frequency to quarterly for ground water systems if a recent sanitary survey shows that the system is free of sanitary defects. Some types of systems can qualify for annual monitoring.
Systems using surface water, rather than ground water, are required to take extra steps to protect against bacterial contamination because surface water sources are more vulnerable to such contamination. At a minimum, all systems using surface waters must disinfect.
In 2006, EPA issued a new rule to ensure that systems using ground water sources take action to treat their drinking water to address microbial contamination if it is identified as a problem. Disinfection will kill E. coli O157:H7.
For more information on treatment visit EPA's microbial pathogens and disinfection byproducts web site.
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What can I do to protect myself from E. coli O157:H7 in drinking water?
Approximately 89 percent of Americans are receiving water from community water systems that meet all health-based standards. Your public water system is required to notify you if, for any reason, your drinking water is not safe. If you wish to take extra precautions, you can boil your water for one minute at a rolling boil, longer at higher altitudes. To find out more information about your water, see the Consumer Confidence Report from your local water supplier or contact your local water supplier directly.
You can also obtain information about your local water system on EPA's web site.
EPA's emergency disinfection of drinking water page
The Centers for Disease Control and Prevention (CDC) suggests other actions that you may take to prevent E. coli infection. These include:
Avoid swallowing lake or pool water while swimming.
Thoroughly cook ground beef and avoid unpasteurized milk.
Make sure that persons with diarrhea, especially children, wash their hands carefully with soap after bowel movements to reduce the risk of spreading infection, and that persons wash hands after changing soiled diapers. Anyone with a diarrhea illness should avoid swimming in public pools or lakes, sharing baths with others, and preparing food for others.
Cook all ground beef and hamburger thoroughly. Because ground beef can turn brown before disease-causing bacteria are killed, use a digital instant-read meat thermometer to ensure thorough cooking. Ground beef should be cooked until a thermometer inserted into several parts of the patty, including the thickest part, reads at least 160º F. Persons who cook ground beef without using a thermometer can decrease their risk of illness by not eating ground beef patties that are still pink in the middle.
If you are served an undercooked hamburger or other ground beef product in a restaurant, send it back for further cooking. You may want to ask for a new bun and a clean plate, too.
Avoid spreading harmful bacteria in your kitchen. Keep raw meat separate from ready-to-eat foods. Wash hands, counters, and utensils with hot soapy water after they touch raw meat. Never place cooked hamburgers or ground beef on the unwashed plate that held raw patties. Wash meat thermometers in between tests of patties that require further cooking.
Drink only pasteurized milk, juice, or cider. Commercial juice with an extended shelf-life that is sold at room temperature (e.g. juice in cardboard boxes, vacuum sealed juice in glass containers) has been pasteurized, although this is generally not indicated on the label. Juice concentrates are also heated sufficiently to kill pathogens.
Wash fruits and vegetables thoroughly, especially those that will not be cooked. Children under 5 years of age, immunocompromised persons, and the elderly should avoid eating alfalfa sprouts until their safety can be assured. Methods to decontaminate alfalfa seeds and sprouts are being investigated.
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Will a water filter work to keep E. coli out of my water?
Most in-home filters will not. EPA recommends that you boil your water if you are concerned about its safety.
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If you have a private drinking water well
If you draw water from a private well, you can contact your state health department to obtain information on how to have your well tested for total coliforms and E. coli contamination. If your well tests positive for E. coli, there are several steps that you should take:
begin boiling all water intended for consumption,
disinfect the well according to procedures recommended by your local health department, and
monitor your water quality to make certain that the problem does not recur.
If the contamination is a recurring problem, you should investigate the feasibility of drilling a new well or install a point-of-entry disinfection unit, which can use chlorine, ultraviolet light, or ozone.
Other resources on private wells
EPA's private drinking water wells web site
EPA's emergency disinfection of drinking water page
EPA's What to do after a flood for steps to disinfect your private drinking water well.
Centers for Disease Control and Prevention (CDC) suggests other actions you may take to prevent E. coli infection.
If I have a private well, how can I have it tested for E. coli?
If you have a private well, you should have your water tested periodically. Contact your State laboratory certification officer to find out which laboratories have been certified for conducting total coliform analyses. (You may contact the Safe Drinking Water Hotline at 1-800-426-4791 for the address and phone number of this individual.) Then contact a certified lab near you and get instructions on how to send them a water sample. Typically, the lab will first test for total coliforms, which is a group of related organisms that is common in both the environment and in the gut of animals. If the sample is positive for total coliforms, the lab will determine whether E. coli is also present. E. coli is a type of total coliform that is closely associated with recent fecal contamination. Few E. coli strains cause disease. However, the presence of any E. coli in a water sample suggests that disease-causing organisms, are also likely to be present.
One of the strains of E. coli that causes disease is E. coli O157:H7. EPA does not believe it necessary for an owner of a private well to test specifically for this organism under normal circumstances. If E. coli O157:H7 is present in your well, it is highly likely that other strains of E. coli are also present. If a well is E. coli-positive, regardless of strain, you should not drink the water unless it is disinfected. Several tests are available for determining whether E. coli O157:H7 is present, but they are somewhat more expensive than the standard E. coli tests and many labs may not have the expertise or supplies to perform these tests. Your state's laboratory certification officer should be able to tell you which laboratories can perform these tests, or you can contact the lab directly.
List of state laboratory certification officers
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If my well is contaminated with E. coli, what can I do to protect myself?
If your well tests positive for E. coli, do not drink the water unless you boil it for at least one minute at a rolling boil, longer if you live at high altitudes. You may also disinfect the well according to procedures recommended by your local health department. Monitor your water periodically after disinfection to make certain that the problem does not recur. If the contamination is a recurring problem, you should investigate the feasibility of drilling a new well or install a point-of-entry disinfection unit, which can use chlorine, ultraviolet light, or ozone.
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1 More than 5.0% samples total coliform-positive in a month. (For water systems that collect fewer than 40 routine samples per month, no more than one sample can be total coliform-positive per month.) Every sample that has total coliform must be analyzed for either fecal coliforms or E. coli if two consecutive TC-positive samples, and one is also positive for E.coli fecal coliforms, system has an acute MCL violation.
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2 Fecal coliform and E. coli are bacteria whose presence indicates that the water may be contaminated with human or animal wastes. Disease-causing microbes (pathogens) in these wastes can cause diarrhea, cramps, nausea, headaches, or other symptoms. These pathogens may pose a special health risk for infants, young children, and people with severely compromised immune systems.
مهم ترین بیماریهای قابل انتقال از حیوان به انسان
مهم ترین و متداولترین بیماریهای قابل انتقال بین حیوان و انسان در كشور ما هاری، كیست هیداتیك، تب مالت، سیاه زخم و ... است كه می توان به آنها اشاره كرد. البته بیماریهایی همچون جنون گاوی، تب کریمه کنگو و آنفلوآنزای پرندگان را نیز نباید نادیده بگیریم، چرا كه خطر ورود و شیوع آنها همواره ما را تهدید می كند.
تا كنون850 بیماری قابل انتقال بین حیوان و انسان شناسایی شده است. تعجب نكنید این رقمی است كه مطمئناً در سالهای بعد بیشتر و بیشتر خواهد شد.
با توجه به اهمیت این بیماریها، اطلاع رسانی و ارتقای سطح آگاهی جامعه در این زمینه از اهمیت ویژه ای برخوردار است. اغلب كارشناسان و متخصصان دامپزشكی با بیان این مطلب كه هر روز بر تعداد افرادی كه به نگهداری حیوانات خانگی رو می آورند، اضافه می شود، تأكید می كنند: در تمام جوامع مهم ترین مشكلی كه در این زمینه مطرح می شود، مسئله ی بیماریهای مشترك بین حیوان و انسان است.
به هر حال نگهداری حیوان در منزل بیشتر از آنكه نفع داشته باشد، ضرر دارد. اصولا زندگی انسان و حیوان در كنار یكدیگر با توجه به مسائل بهداشتی نمی تواند ایدهای مناسب باشد. بسیاری از بیماریها بین انسان و حیوان مشترك هستند و به راحتی از حیوان به انسان سرایت می كند.
در بعضی از موارد بیماری خاصی در حیوان می تواند انسان را از پا در آورد. موارد دیگری نیز وجود دارد كه ثابت می كند، حیوان نمی تواند در محیطی زندگی كند كه انسان در آن قدم گذاشته است. به عنوان مثال ریزش موی گربه می تواند حساسیتی خطرناك را در انسان به همراه داشته باشد.
فراموش نكنیم انسان و حیوان وجه مشتركی در بهداشت ندارند، چون حیوان فاقد شعور و درك است و برایش فرقی نمی كند كه در ظرف غذای شما اجابت مزاج كند یا در توالت فرنگی!
مهم ترین بیماریهای قابل انتقال از حیوان به انسان در كشور ما عبارتند از:
بسیاری از مردم بر این باورند كه انسان تنها از طریق گاز گرفتن سگ هار به بیماری هاری مبتلا می شود، در حالی كه گاز گرفتن حیواناتی همچون گربه، خفاش، موش و گرگ نیز می تواند منجر به هاری شود. به تازگی در شمال ایران راكونهای زیادی مشاهده شدهاند كه از طریق كشورهای همسایه ی شمالی وارد جنگلهای ایران شدهاند و خود اینها به عنوان یك مخزن هاری به حساب می آیند.
در مورد هاری بهترین راه پیشگیری واكسیناسیون حیوانات خانگی است. البته در سالهای اخیر برای واكسینه كردن حیوانات وحشی مانند سگهای ولگرد كه به صورت دسته جمعی در اطراف شهرها دیده می شوند نیز اقداماتی صورت گرفته است. به هر حال اگر انسانی توسط حیوانی مشكوك گاز گرفته شد، باید بلافاصله از سرم ضد هاری استفاده شود و به یاد داشته باشید كه تزریق به موقع این سرم می تواند از مرگ فرد جلوگیری كند.
* كیست هیداتیك:
ایجاد كیست هیداتیك در اثر ورود تخمهای انگل اكینوكوكوس (موجود در مدفوع سگ) به دستگاه گوارش انسان صورت می گیرد. این كیستها بسته به اینكه در ریه، كبد، مغز یا هر بافت دیگری ایجاد شده باشند، قادر به بروز عوارض مختلفی هستند و برای برداشتن آنها نیاز به عمل جراحی است.
درمان ضد انگل دورهای حیوان خانگی (سگ)، رعایت بهداشت فردی و نیز ضدعفونی كردن سبزیجات مصرفی از موارد پیشگیری است.
انگل خونی توكسوپلاسموز در اكثر گربههای ولگرد مشاهده می شود و در صورت خارج شدن گربه ی خانگی از منزل و معاشرت با گربههای ولگرد احتمال آلوده شدن آن بسیار است. چنین گربه ای باید به صورت دورهای تحت درمان باشد. اگر چه در انسان عوارض آن خفیف است، ولی در خانمهای باردار می تواند منجر به سقط جنین شود.
* بیماری خراش پنجه ی گربه:
به طور معمول، زیر ناخن گربه یك سری میكروب وجود دارد كه در صورت چنگ زدن گربه، این میکروب ها از طریق خراش وارد بدن شده و باعث بروز این بیماری می شوند. دراین بیماری انسان تا 3 روز متوالی تب می كند و گاهی نیز دچار تهوع و سردرد می شود.
* سل و تب مالت:
سل و تب مالت(بروسلوز) دو بیماری خطرناك و از جمله بیماریهایی هستند كه برای سازمان دامپزشكی در صدر مهار بیماری ها قرار گرفتهاند. این بیماریها از طریق دام آلوده (خصوصاً گاو و گوسفند) به انسان منتقل می شوند. سل قابلیت انتقال از انسان به انسان (در انواع مختلف) را دارد و باکتری بروسلا باعث ایجاد تب مالت در انسان می شود.
واكسینه كردن دامها علیه این دو بیماری یك طرح ملی است. استفاده از شیر و لبنیات پاستوریزه مهم ترین راه پیشگیری است. اما اگر در جایی ناگریز به استفاده از شیر غیر پاستوریزه باشیم، عمل جوشاندن دقیق شیر كمك زیادی به ما خواهد كرد. فراموش نكنید در فصل تابستان موارد ابتلا به تب مالت بر اثر مصرف بستنیهای غیرپاستوریزه، افزایش می یابد.
* تب طوطی:
تب طوطی نوعی بیماری است كه از طریق پرندگان گروه منقار طوطیها به انسان منتقل می شود. البته دیگر پرندگان نیز در صورت ابتلا به تب روده (به خصوص در تابستان)، با دفع باكتری "سالمونلا" از طریق مدفوع می توانند موجب به خطر افتادن سلامتی انسانها، خصوصا افراد ضعیف و بچهها شوند.
خوشبختانه این بیماری درمان پذیر است و بیشتر در اثر عدم رعایت بهداشت در اماكنی همچون رستورانها به انسان منتقل می شود.
* طاعون و انواع بیماریهای انگلی:
موشها، عوامل باكتریایی و انگلی بسیاری را به انسان منتقل می كنند و باعث ایجاد بیماریهای بعضاً كشنده می شوند و تنها كشتار دستهجمعی این حیوانات به پیشگیری از این بیماریها كمك می كند.
از زمان قدیم انسان هر جا مواد غذایی را نگهداری می كرد، همواره با موشها درگیر بوده است. هرگاه ادرار و مدفوع آلودهی موش با مواد غذایی مورد استفاده ی انسان تماس پیدا كند، موجب ابتلا شخص به بیماریهای مختلف می شود