Escherichia coli enteritis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.; Serge Korjian M.D.

E. coli enteritis is an infectious bacterial gastroenteritis caused by a pathogenic strain of the Gram-negative rod, Escherichia coli. It is one of the most common causes of diarrhea worldwide and is responsible for 20% to 50% of all infectious diarrhea, with an incidence in the USA of approximately 20-30 cases per 100,000 individuals. E. coli enteritis may be classified according to the causative E. coli strain into Enterotoxigenic E. coli (ETEC), Enteropathogenic E. coli (EPEC), Enterohemorrhagic E. coli (EHEC), Enteroinvasive E. coli (EIEC), and Enteroaggressive E. coli (EAEC). Transmission of pathogenic E. coli strains is usually by the fecal-oral route in contaminated foods and water. The pathogenesis by which each E. coli strain causes clinical manifestations is unique: ETEC, EHEC, and EAEC secrete toxins, EIEC invades the host colonocytes and migrates within cells, whereas EPEC uses EPEC-elongation factor (EAF) to cause “attachment and effacing”. Risk factors in the development of E. coli enteritis include young and old age, immunocompromised status, pregnancy, recent ingestion of uncooked or poorly handled vegetables, meat (e.g. hamburgers), poultry, raw milk, or poorly stored foods that require refrigeration (e.g. mayonnaise), drinking from untreated water, recent travel to developing countries, exposure to infected individuals, daycare, and healthcare settings, and recent sexual history of receptive anal or oral–anal contact. Following transmission, the incubation period of pathogenic E. coli strains is approximately 1-10 days, during which the infected patient remains asymptomatic. Early manifestations of E. coli enteritis include diffuse abdominal pain, vomiting, and severe acute watery diarrhea, which may be followed by episodes of bloody diarrhea (in EHEC and EIEC infections). The majority of patients report resolution of symptoms within 5-10 days of symptom-onset. Common complications of E. coli enteritis include hemolytic uremic syndrome (in EHEC infection), thrombotic thrombocytopenic purpura (in EHEC infection), and acute kidney injury. Prognosis of E. coli enteritis is generally excellent, and the majority of cases resolve without any long-term sequelae. Identification of the causative strain is usually not necessary for diagnosis and treatment. Diagnostic laboratory tests may include either stool culture, ELISA, or polymerase chain reaction (PCR). Rehydration is the mainstay of therapy of E. coli enteritis. Oral rehydration fluids (e.g. oral rehydration solutions) are indicated among patients who can tolerate oral intake, otherwise IV rehydration is indicated. Since the majority of cases of E. coli enteritis are self-limited and the exact infective strain is often not identified, empiric antimicrobial therapy is generally not recommended. Antimicrobial therapy, using either fluoroquinolone or TMP-SMX may be administered (but is not required) in ETEC infection, EPEC infection, and EIEC infection, but not in EHEC infection. Effective preventive measures include hand washing using soap and water and proper food handling.

Theodor Escherich, a German physician, was the first to grow cultures of E. coli in 1885. The first pathogenic E. coli strain described was enteropathogenic E. coli (EPEC). The infection was reported in 1945 following outbreaks of infant diarrhea in the United Kingdom.^[1]

E. coli enteritis may be classified according to the causative E. coli strain into Enterotoxigenic E. coli (ETEC), Enteropathogenic E. coli (EPEC), Enterohemorrhagic E. coli (EHEC), Enteroinvasive E. coli (EIEC), and Enteroaggressive E. coli (EAEC).

E. coli normally colonizes the human gastrointestinal tract shortly following birth. However, the colonizing E.coli strains are different from the pathogenic strains. Transmission of pathogenic E. coli strains is usually by the fecal-oral route via infected food products (e.g. under cooked beef, vegetables, unpasteurized milk products or juice), contaminated water, infected cattle, or human fecal material (e.g. oral–anal contact). Only enteroinvasive E. coli (EIEC) has true replication within the host cell, whereas all other types of E. coli replicate outside the host cell. The small intestine is the primary site of action of ETEC and EPEC, whereas the colon is the primary site of action of EHEC and EIEC. EAEC may act on either enterocytes or colonocytes. The pathogenesis, by which each E. coli strain causes manifestations, is unique: ETEC, EHEC, and EAEC secrete toxins, EIEC invades the host colonocytes and migrates within cells, whereas EPEC uses EPEC-elongation factor (EAF) to cause “attachment and effacing”. Finally, the diffusely adherent E. coli strain (DAEC) is a subtype of EPEC that utilizes unique patterns of adherence.

E. coli enteritis is caused by pathogenic strains of the bacterium Escherichia coli. E. coli is a non-spore-forming, glucose–fermenting, catalase-positive, lactose-positive, mannitol-positive, oxidase-negative, cellobiose-negative, facultatively anaerobic, Gram-negative rod.

E. coli enteritis must be differentiated from other causes of abdominal pain, diarrhea, and fever (less common), such as other infectious causes of gastroenteritis, including bacterial, viral, fungal, and parasitic pathogens, in addition to non-infectious causes, including acute pancreatitis, appendicitis, bowel obstruction, diverticulitis, drug reaction, hyperthyroidism, inflammatory bowel disease, mesenteric ischemia, peritonitis, and pneumonia.

E. coli is one of the most common causes of diarrhea worldwide and is responsible for 20% to 50% of all infectious diarrhea. The exact incidence of E. coli enteritis is difficult to estimate, but it is thought that E. coli causes more than 500-700 million cases of enteritis and is responsible for approximately 700,000 deaths each year. In the USA, the incidence of E. coli enteritis is estimated to be approximately 20-30 cases per 100,000 individuals. Young children < 5 years of age and elderly individuals are more commonly affected with E. coli enteritis. There is no gender or racial predilection to the development of E. coli enteritis. E. coli enteritis is more common in developing countries than in developed countries.

Risk factors in the development of E. coli enteritis include young and old age, immunocompromised status, pregnancy, recent ingestion of uncooked or poorly handled vegetables, meat (e.g. hamburgers), poultry, raw milk, or poorly stored foods that require refrigeration (e.g. mayonnaise), drinking from untreated water, recent travel to developing countries, exposure to infected individuals, daycare, and healthcare settings, and recent sexual history of receptive anal or oral–anal contact.

Screening asymptomatic individuals for the presence of enteritis-causing E. coli strains is not recommended.

Following transmission, the incubation period of pathogenic E. coli strains is approximately 1-10 days, during which the infected patient remains asymptomatic. Early manifestations of E. coli enteritis include diffuse abdominal pain, vomiting, and severe acute watery diarrhea, which may be followed by episodes of bloody diarrhea (in EHEC and EIEC infections). The majority of patients report resolution of symptoms within 5-10 days of symptom-onset. Common complications of E. coli enteritis include hemolytic uremic syndrome (in EHEC infection), thrombotic thrombocytopenic purpura (in EHEC infections), and acute kidney injury. Prognosis of E. coli enteritis is generally excellent, and the majority of cases resolve without any long-term sequelae.

Symptoms of E. coli enteritis include diarrhea (either watery or bloody), nausea, vomiting, abdominal pain, and bloating with or without fever (fever is characteristically absent in EHEC enteritis, but may be present in enteritis caused by other E. coli strains). Less common symptoms may be related to complications of E. coli enteritis, such as hemolytic uremic syndrome, and may include spontaneous bruising, oliguria/anuria, and painless gross hematuria.

Physical examination of patients with E. coli enteritis may be remarkable for abdominal tenderness, fever (occasionally), and signs of dehydration, such as abnormal orthostatic vital signs, reduced skin turgor, slow capillary refill, and dry mucous membranes. Physical examination among patients with severe dehydration may be remarkable for altered mental status. Physical examination may also be remarkable for findings suggestive of complications of the E. coli enteritis (e.g. hemolytic uremic syndrome), such as skin pallor, petechiae, and bruises.

Identification of the causative strain is usually not necessary for diagnosis and treatment. Diagnostic laboratory tests for E. coli enteritis usually include either stool culture, ELISA, or polymerase chain reaction (PCR). Other laboratory findings in E. coli enteritis are usually non-specific and may include increased white blood cell count and elevated inflammatory markers. Laboratory findings suggestive of dehydration may include relative polycythemia, metabolic alkalosis, elevated BUN and serum creatinine (suggestive of pre-renal acute kidney injury). When hospitalized, patients should also be monitored for laboratory findings that may suggest development of hemolytic uremic syndrome, such as hemolytic anemia, elevated serum creatinine, and thrombocytopenia.

Rehydration is the mainstay of therapy of E. coli enteritis. Oral rehydration fluids (e.g. oral rehydration solutions) are indicated among patients who can tolerate oral intake, otherwise IV rehydration is indicated. Since the majority of cases of E. coli enteritis are self-limited and the exact infective strain is often not identified, empiric antimicrobial therapy is generally not recommended. Antimicrobial therapy using either fluoroquinolone or TMP-SMX may be administered (but is not required) in ETEC infection (traveler’s diarrhea), EPEC infection, and EIEC infection, but not in EHEC infection (due to increased risk of hemolytic uremic syndrome and prolonged shedding). In adults, additional pharmacologic therapies may include antiemetic agents (not recommended in pediatric patients). Antidiarrheal agents are generally not recommended during the acute infection phase.

Surgery is not recommended to treat E. coli enteritis.

According to the Centers for Disease Control and Prevention (CDC), preventive measures against development of E. coli enteritis include applying proper hand hygiene using soap and water, cooking meat thoroughly (to a temperature of at least 160°F / 70˚C), avoiding consumption of raw and unpasteurized products (e.g. milk, other dairy products, and juices), and avoiding swallowing water when swimming.^[2]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Serge Korjian M.D., Yazan Daaboul, M.D.

Theodor Escherich, a German physician, was the first to grow cultures of E. coli in 1885. The first pathogenic E. coli strain described was enteropathogenic E. coli (EPEC). The infection was reported in 1945 following outbreaks of infant diarrhea in the United Kingdom.^[1]

• Theodor Escherich, a German physician, was the first to grow cultures of E. coli in 1885.
• Prior to reports of pathogenicity, all strains of E. coli were first thought to be part of the normal flora. The first pathogenic E. coli strain described was enteropathogenic E. coli (EPEC). The infection was reported in 1945 following outbreaks of infant diarrhea in the United Kingdom.^[1]
• The majority of advances in understanding the pathogenesis of enteropathogenic E. coli infection were made in the late 1970s / early 1980s.^[2]
• Subsequently, other pathogenic E. coli strains were described in the early 1980s: EHEC (enterohemorrhagic E. coli)then ETEC (enterotoxicogenic E. coli) and then followed by EIEC (enteroinvasive E. coli) and finally DAEC (diffusely adherent E. coli).^[2]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Serge Korjian M.D., Yazan Daaboul, M.D.

E. coli enteritis may be classified according to the E. coli species into Enterotoxigenic E. coli (ETEC), Enteropathogenic E. coli (EPEC), Enterohemorrhagic E. coli (EHEC), Enteroinvasive E. coli (EIEC), and Enteroaggressive E. coli (EAEC).

E. coli enteritis may be classified according to the involved E. coli species listed as follows:

• Enterotoxigenic E. coli (ETEC)
• Enteropathogenic E. coli (EPEC) (including diffusely adherent E. coli [DAEC], a subtype of EPEC)
• Enterohemorrhagic E. coli (EHEC) (may be Shiga-like toxin producing or Verotoxin-producing)
• Enteroinvasive E. coli (EIEC)
• Enteroaggressive E. coli (EAEC)

The following table demonstrates the distinguishing clinical features and pathophysiological mechanisms of various enteritis-causing E. coli strains:

^{a=LT, labile toxin; ST, stable toxin; b=ID, infective dose.
Adapted from Food and Drug Administration (FDA) – Bacteriological Analytical Manual Chapter 4A – Diarrheagenic Escherichia coli.[1]}

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.; Serge Korjian M.D.

E. coli normally colonizes the human gastrointestinal tract shortly following birth. However, the colonizing E.coli strains are different from the pathogenic strains. Transmission of pathogenic E. coli strains is usually by the fecal-oral route via infected food products (e.g. undercooked beef, vegetables, unpasteurized milk products or juice), contaminated water, infected cattle, or human fecal material (e.g. oral–anal contact). Only enteroinvasive E. coli (EIEC) has true replication ability within the host cell, whereas all other types of E. coli replicate outside the host cell. The small intestine is the primary site of action of ETEC and EPEC, whereas the colon is the primary site of action of EHEC and EIEC. EAEC may act on either enterocytes or colonocytes. The pathogenesis by which each E. coli strain causes manifestations is unique. For example, ETEC, EHEC, and EAEC secrete toxins, EIEC invades the host colonocytes and migrates within cells, whereas EPEC uses EPEC-elongation factor (EAF) to cause “attachment and effacing”. Finally, DAEC is a subtype of EPEC that utilizes unique patterns of adherence.

• E. coli normally colonizes the human gastrointestinal tract shortly following birth and is part of the normal gastrointestinal flora. However, the colonizing E.coli strains are different from the pathogenic strains that cause E. coli enteritis.

• Transmission of pathogenic E. coli strains is usually by the fecal-oral route via the following:

• Contaminated food, especially under cooked ground beef, unpasteurized (raw) milk and juice, soft cheeses made from raw milk, and raw fruits and vegetables (such as sprouts)
• Contaminated water, including drinking untreated water and swimming in contaminated water
• Animals (particularly cows, sheep, and goats) and their environment
• Feces of infected people (e.g. oral–anal contact)

• Pathogenic E. coli are characterized by the presence of either O antigen alone or combination of O and H antigens.^[1][2]

• O antigen corresponds to the lipopolysaccaride antigen
• H antigen corresponds to the flagellar antigen

• Only enteroinvasive E. coli (EIEC) has true replication within the host cell, whereas all other types of E. coli replicate outside the host cell.^[1]
• Pathogenic E. coli strains contain adhesin that may form distinct fimbriae (pili) or fibrillae.

• The primary site of action of ETEC is the small intestine.
• ETEC adheres to enterocytes then secretes 2 enterotoxins: heat-labile toxin (LT) and heat-stable toxin (ST).^[2]
• Both enterotoxins are responsible for the development of clinical manifestations (e.g. diarrhea).^[1]

• Heat-labile toxin is composed of one enzymatically active subunit and 5 surrounding inactive subunits. It induces diarrhea by binding to GM1 receptor, the same ganglioside receptor that the cholera toxin of V. cholerae binds to.^[2]
• Heat-stable toxin is composed of several peptides that are not inactivated by heat. It binds to and activates guanylate cyclase, resulting in diarrhea by increasing secretion of fluids and electrolytes.^[2]

• The primary site of action of EHEC is the colon.
• EHEC attaches to the colonocyte and causes hemorrhagic colitis by inducing the elaboration of the Shiga toxin (Stx) and secretion of enterohemolysin.
• The Shiga toxin is systemically absorbed and results in inflammatory reactions and systemic complications, including hemolytic uremic syndrome.
• EHEC are not considered highly invasive as EIEC or Shigella because the organism invades the cell but does not multiply within the cell.^[1][2]

• The primary site of action of EIEC is the colon.
• EIEC is invasive and multiplies within the host colonocytes.
• EIEC contains nonfimbrial adhesins. It lyses phagosomes and migrates through the host cell and within cells (either lateral direct cell-to-cell spread or exit then re-enter) via the action of nucleating actin microfilaments.^[1][2]

• The primary site of action of EAEC is the small intestine and the colon.
• EAEC is characteristically aggressive and adheres to enterocytes and colonocytes in a thick biofilm.
• EAEC elaborates cytotoxins, such as hemolysin, and enterotoxins, such as ShET1, Pic, EAST1, Pet toxins.^[1][2]

• The primary site of action of EPEC is the small intestine.
• EPEC contains EPEC-adherence factor (EAF), a plasma encoded protein.
• Using EAF, EPEC adheres to enterocytes and destroy the normal architecture of the human microvilli, resulting in cytoskeletal deformities. The process is referred to as “attachment and effacing”.^[1][2]
• Similar to EHEC, it is not considered highly invasive.^[1][2]

• DAEC is a subtype of EPEC, which contains unique patterns of adherence.^[1][2]

This page is about microbiologic aspects of the organism. To view a list of E. coli organ-based infections, click here.
To view specific information about E. coli O157:H7 strain, click here.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Escherichia coli (Template:PronEng) (E. coli), is a bacterium that is commonly found in the lower intestine of warm-blooded animals. Most E. coli strains are harmless, but some, such as serotype O157:H7, can cause serious food poisoning in humans, and are occasionally responsible for costly product recalls.^[1][2] The harmless strains are part of the normal flora of the gut, and can benefit their hosts by producing vitamin K₂, or by preventing the establishment of pathogenic bacteria within the intestine.^[3][4][5]

E. coli is not always confined to the intestine, and its ability to survive for brief periods outside the body makes it an ideal indicator organism to test environmental samples for fecal contamination.^[6][7] The bacteria can also be grown easily and its genetics are comparatively simple and easily-manipulated, making it one of the best-studied prokaryotic model organisms, and an important species in biotechnology. E. coli was discovered by a German pediatrician and bacteriologist Theodor Escherich in 1885, and is now classified as part of the Enterobacteriaceae family of gamma-proteobacteria.^[6][8]

A strain of E. coli is a sub-group within the species that has unique characteristics distinguishing it from other E. coli strains. These differences are often detectable only on the molecular level; however, they may result in changes to the physiology or life cycle of the bacterium. For example, a strain may gain pathogenic capacity, the ability to use a unique carbon source, the ability to inhabit a particular ecological niche, or the ability to resist antimicrobial agents. Different strains of E. coli are often host-specific, making it possible to determine the source of fecal contamination in environmental samples. Depending on which E. coli strains are present in a water sample, for example, assumptions can be made about whether the contamination originated from a human, other mammal, or bird source.

New strains of E. coli evolve through the natural biological process of mutation, and some strains develop traits that can be harmful to a host animal. Although virulent strains typically cause no more than a bout of diarrhea in healthy adult humans, particularly virulent strains, such as O157:H7 or O111:B4, can cause serious illness or death in the elderly, the very young, or the immunocompromised.^[4]

E. coli is Gram-negative, facultative anaerobic and non-sporulating. It can live on a wide variety of substrates. E. coli uses mixed-acid fermentation in anaerobic conditions, producing lactate, succinate, ethanol, acetate, and carbon dioxide. Since many pathways in mixed-acid fermentation produce hydrogen gas, these pathways require the levels of hydrogen to be low, as is the case when E. coli lives together with hydrogen-consuming organisms such as methanogens or sulfate-reducing bacteria.^[9]

Optimal growth of E. coli occurs at 37°C, but some laboratory strains can multiply at temperatures of up to 49°C.^[10] Growth can be driven by aerobic or anaerobic respiration, using a large variety of redox pairs, including the oxidation of pyruvic acid, formic acid, hydrogen and amino acids, and the reduction of substrates such as oxygen, nitrate, dimethyl sulfoxide and trimethylamine N-oxide.^[11]

Strains that possess flagella can swim and are motile, but other strains lack flagellum. The flagella of E. coli have a peritrichous arrangement.^[12]

E. coli and related bacteria possess the ability to transfer DNA via bacterial conjugation, transduction or transformation, which allows genetic material to spread horizontally through an existing population. It is believed that this process led to the spread of shiga toxin from Shigella to E. coli O157:H7.

E. coli normally colonizes an infant’s gastrointestinal tract within 40 hours of birth, arriving with food or water or from the individuals handling the child. In the bowel, it adheres to the mucus of the large intestine. It is the primary facultative organism of the human gastrointestinal tract.^[13] As long as these bacteria do not acquire genetic elements encoding for virulence factors, they remain benign commensals.^[14]

Virulent strains of E. coli can cause gastroenteritis, urinary tract infections, and neonatal meningitis. In rarer cases, virulent strains are also responsible for peritonitis, mastitis, septicemia and Gram-negative pneumonia.^[13] Recently it is thought that E. coli and certain other foodborne illnesses can sometimes trigger serious health problems months or years after patients survived that initial bout. Food poisoning can be a long-term problem.

Enteric E. coli (EC) are classified on the basis of serological characteristics and virulence properties.^[13]

Virotypes include:

• Enterotoxigenic E. coli (ETEC) – It is the causative agent of diarrhea (without fever) in humans, pigs, sheep, goats, cattle, dogs, and horses. ETEC uses fimbrial adhesins (projections from the bacterial cell surface) to bind enterocytes in the small intestine. ETEC can produce two proteinaceous enterotoxins: the larger of the two proteins, LT enterotoxin, is similar to cholera toxin in structure and function, while the smaller protein, ST enterotoxin causes cGMP accumulation in the target cells and a subsequent secretion of fluid and electrolytes into the intestinal lumen. ETEC strains are non-invasive, and they do not leave the intestinal lumen.
• Enteropathogenic E. coli (EPEC) – It is the causative agent of diarrhea in humans, rabbits, dogs, cats and horses. Like ETEC, EPEC also causes diarrhea, but the molecular mechanism of colonization and etiology are different. EPEC lack fimbriae, ST and LT toxins, but they utilize an adhesin known as intimin to bind host intestinal cells. This virotype has an array of virulence factors that are similar to those found in Shigella, and may posses a shiga toxin. Adherence to the intestinal mucosa causes a rearrangement of actin in the host cell, causing significant deformation. EPEC cells are moderately-invasive (i.e. they enter host cells) and elicit an inflammatory response. Changes in intestinal cell ultrastructure due to “attachment and effacement” is likely the prime cause of diarrhea in those afflicted with EPEC.
• Enteroinvasive E. coli (EIEC) – It is found only in humans. EIEC infection causes a syndrome that is identical to Shigellosis, with profuse diarrhea and high fever. EIEC are highly invasive, and they utilize adhesin proteins to bind to and enter intestinal cells. They produce no toxins, but can cause severe damage to the intestinal wall through mechanical cell destruction.
• Enterohemorrhagic E. coli (EHEC) – It is found in humans, cattle, and goats. The sole member of this virotype is strain O157:H7, which causes bloody diarrhea and no fever. EHEC can cause hemolytic uremic syndrome and sudden kidney failure. It uses bacterial fimbriae for attachment and is moderately invasive. It possesses a phage-encoded Shiga toxin that can elicit an intense inflammatory response.
• Enteroaggregative E. coli (EAggEC) – It is found only in humans. This strain is named “aggregative” because their fimbriae aggregate tissue culture cells. EAggEC binds to the intestinal mucosa while being non-invasive and causes watery diarrhea without fever. It produces a hemolysin and an ST enterotoxin similar to that of ETEC.

Certain strains of E. coli, such as O157:H7, O121 and O104:H21, produce toxins. Food poisoning caused by E. coli are usually associated with eating unwashed vegetables and meat contaminated post-slaughter. O157:H7 is further notorious for causing serious and even life-threatening complications such as Hemolytic Uremic Syndrome (HUS). This particular strain is linked to the 2006 United States E. coli outbreak of fresh spinach and the most recent multistate outbreak linked to romaine lettuce from the Central Coastal growing regions in northern and central California. Severity of the illness varies considerably; it can be fatal, particularly to young children, the elderly, or the immunocompromised, but is more often mild. E. coli can harbor both heat-stable and heat-labile enterotoxins. The latter, termed LT, contains one ‘A’ subunit and five ‘B’ subunits arranged into one holotoxin, and is highly similar in structure and function to Cholera toxins. The ‘B’ subunits assist in adherence and entry of the toxin into host intestinal cells, while the ‘A’ subunit is cleaved and prevents cells from absorbing water, causing diarrhea. LT is secreted by the Type 2 secretion pathway.^[15]

If E. coli escapes the intestinal tract through a perforation (for example from an ulcer, a ruptured appendix, or a surgical error) and enters the abdomen, it usually causes peritonitis that can be fatal without prompt treatment. E. coli is extremely sensitive to antibiotics such as streptomycin or gentamicin and treatment with these antibiotics is usually effective.E. coli can also quickly acquire drug resistance which can be troublesome.^[16]

Intestinal mucosa-associated E. coli is observed in increased numbers in patients with inflammatory bowel disease such as Crohn’s disease and ulcerative colitis.^[17] Invasive strains of E. coli exist in high numbers in the inflamed tissue, and the number of bacteria in the inflammatory foci correlates with the severity of the bowel inflammation.^[18]

Transmission of pathogenic E. coli often occurs via fecal-oral route. Common sources of contamination include: unhygienic food preparation, farm contamination due to manure fertilization, irrigation of crops with contaminated greywater or raw sewage, feral pigs on cropland, or direct consumption of sewage-contaminated water.^{[19][14][20][21][22][23][24]}

Dairy and beef cattle are the primary reservoirs of E. coli O157:H7. They can carry it while being asymptomatic and shed it in their feces. Food products associated with E. coli outbreaks include raw ground beef, raw seed sprouts or spinach, raw milk, unpasteurized juice, lettuce (as observed in the most recent [October-November 2018] multistate outbreak of Shiga toxin-producing Escherichia coli O157:H7 (E. coli O157:H7) infections linked to romaine lettuce from the Central Coastal growing regions in northern and central California), and foods contaminated by infected food workers via fecal-oral route.^{[19][21][25][26]}

According to the U.S. Food and Drug Administration, the fecal-oral cycle of transmission can be disrupted by cooking food properly, preventing cross-contamination, instituting barriers such as gloves for food workers, pasteurization of juice or dairy, proper hand washing requirements, and instituting health care policies requiring food industry employees to seek medical care when they are ill.^[19]

Shiga toxin-producing E. coli (STEC), specifically serotype O157:H7, can also be transmitted by flies. Tranmission can also occur via direct contact with farm animals, petting zoo animals, and airborne particles found in animal-rearing environments.^{[27][28][29][30][31][32][33]}

Uropathogenic E. coli (UPEC) is responsible for approximately 90% of urinary tract infections (UTI) seen in individuals with ordinary anatomy. In ascending infections, fecal bacteria colonize the urethra and spread up the urinary tract to the bladder. Women are 14-times more likely to suffer from an ascending UTI as compared to men because of the anatomical difference in the urethral length.^[13]

Uropathogenic E. coli utilize P fimbriae (pyelonephritis-associated pili) to bind urinary tract epithelium and colonize the bladder. These adhesins specifically bind D-galactose-D-galactose moieties on the P blood group antigen of erythrocytes and uroepithelial cells. Approximately 1% of the human population lacks this receptor, and its presence or absence dictates an individual’s susceptibility to urinary tract infections caused by E. coli. Uropathogenic E. coli produce alpha- and beta-hemolysins, which cause lysis of urinary tract cells.^[13]

UPEC can evade the body’s innate immune defenses (e.g. the complement system) by invading superficial umbrella cells to form intracellular bacterial communities (IBCs). It can also have the ability to form K antigen and capsular polysaccharides that contribute to biofilm formation. Biofilm-producing E. coli is recalcitrant to immune factors and antibiotic therapy and can be responsible for chronic urinary tract infections. K antigen-producing E. coli commonly cause infection of the upper urinary tract.^[13][34][35]

Descending infections, though relatively rare, occur when E. coli enters the upper urinary tract (kidneys, bladder or ureters) from the blood stream.

Enteropathogenic E. coli (EPEC) and Enterotoxigenic E. coli (ETEC) – UTI or GIT infections in infants are caused by EPEC which present as watery diarrhea, meaning that PMN’s will not be observed in the stool neither with methylene blue nor Gram stain. Gram negative rods, with no particular arrangement, are seen on Gram stain. On MacConkey agar inoculated with stool, deep red colonies are produced as the organism is lactose positive, and this utilization will cause the medium’s pH to drop leading to darkening of the medium. Growth on Levine EMB agar inoculated with stool will show black colonies with greenish-black metallic sheen. This is diagnosic of E. coli. The organism is lysine positive, and grows on TSI slant with a (A/A/g+/H₂S-) profile. IMViC is ++– for E. coli as it is indol positive (red ring) and methyl red positive (bright red), but Voges–Proskauer (VP) negative (no change – colorless) and citrate negative (no change-green color). Serology is done using the SSS-Coagglutination test.

Enterohaemorrhagic E. coli O157:H7 – It is isolated either from urine or, more commonly, stool. There exist three protocols for diagnosis:

1. Diagnosis is made in the manner similar to the diagnostic protocol of EPEC and ETEC. Sorbitol-MacConkey agar, a modified MacConkey agar which has sorbitol instead of lactose, is used and the EHEC produce colorless colonie due to is inability to utilize sorbitol. TSI slant and IMViC are then performed. Serology detects O157:H7 antigens.
2. Gram stain demonstrating gram negative rods with no particular arrangement.
3. Two bottles of verocells are used. One is inoculated with equal portions of stool extract and antitoxin, while the other containing only stool extract. If the first bottle shows neutralization (no cytopathic effects) while the second doesn’t; the test is considered positive. This is based on the fact that the toxin produced by this strain is neutralized in the presence of its specific antibody, meaning that it will not be able to exert its effects on cells.

Bacterial infections are usually treated with antibiotics. However, the antibiotic sensitivities of different strains of E. coli vary widely. As a Gram-negative organism, E. coli is resistant to many antibiotics that are effective against Gram-positive organisms. Antibiotics which may be used to treat E. coli infection include amoxicillin as well as other semi-synthetic penicillins, many cephalosporins, carbapenems, aztreonam, trimethoprim-sulfamethoxazole, ciprofloxacin, nitrofurantoin, and aminoglycosides.

Antibiotic resistance is a growing problem. A part of it is due to the overuse of antibiotics in humans, but the use of antibiotics as growth promoters in the food of animals is also a contributing factor. A study published in the journal Science in August 2007 found that the rate of adaptative mutations in E. coli is on the order of 10^–5 per genome per generation, which is 1,000 times as high as previous estimates. This finding is very significant for the study and management of bacterial antibiotic resistance.^[36][37]

Antibiotic-resistant E. coli may also pass on the genes responsible for antibiotic resistance to other species of bacteria, such as Staphylococcus aureus. E. coli often carry multidrug resistant plasmids and when under stress, it can readily transfer those plasmids to other species. E. coli is a frequent member of biofilms, where many species of bacteria exist in close proximity to each other. This mixing of species allows E. coli strains that are piliated to accept and transfer plasmids from and to other bacteria. Thus, E. coli and the other enterobacteria are important reservoirs of transferable antibiotic resistance.^[38]

Resistance to beta-lactam antibiotics has become a particular problem in the recent decades, as strains of bacteria that produce extended-spectrum beta-lactamases have become more common. The beta-lactamase makes many, if not all, of the penicillins and cephalosporins ineffective as therapeutic measures. Extended-spectrum beta-lactamase–producing E. coli are highly resistant to an array of antibiotics and infections caused by these strains are difficult to treat. In many instances, only two oral antibiotics and a very limited group of intravenous antibiotics remain effective.^[39]

Increased concern about the prevalence of this form of “superbug” in the United Kingdom has led to calls for further monitoring and a UK-wide strategy to deal with infections and the deaths. Susceptibility testing should guide treatment in all infections in which the organism can be isolated for culture.^[40]

Phage therapy involves the use of viruses that specifically target pathogenic bacteria. It has been developed over the last 80 years, primarily in the former Soviet Union, where it was used to prevent diarrhea caused by E. coli. Presently, phage therapy for humans is available only at the Phage Therapy Center in the Republic of Georgia and Poland. However, on January 2 2007, the United States Food and Drug Administration (FDA) gave Omnilytics (a biotech company focused on developing solutions for infectious disease and pest control) the approval to apply its E. coli O157:H7 killing phage in a mist, spray, or wash on live cattle bred for harvest.^{[41][42] [43]}

Researchers have actively been working to develop safe, effective vaccines to lower the worldwide incidence of E. coli infection. In March, 2006, a vaccine, eliciting an immune response against the E. coli O157:H7 O-specific polysaccharide conjugated to recombinant exotoxin A of Pseudomonas aeruginosa (O157-rEPA), was reported to be safe in children two to five years old. Previous work had already indicated its safety in adults. A phase III clinical trial to verify the large-scale efficacy of the treatment is planned.^[44][45]

In January 2007 the Canadian bio-pharmaceutical company Bioniche announced the development of a cattle vaccine which reduces the number of E. coli O157:H7 shed in manure to about 1000 pathogenic bacteria per gram of manure.^[46][47][48]

File:E coli metabolic network.png

Because of its long history of laboratory culture and ease of manipulation, E. coli also plays an important role in modern biological engineering and industrial microbiology. The work of Stanley Norman Cohen and Herbert Boyer on E. coli, using plasmids and restriction enzymes to create recombinant DNA, has become a foundation.^{[49] [50]}

E. coli is considered a very versatile host for the production of heterologous proteins. Researchers can introduce genes into the microbes using plasmids, allowing for the mass production of proteins used in the industrial fermentation processes. Genetic systems have also been developed which allow the production of recombinant proteins using E. coli. One of the first useful applications of recombinant DNA technology was the manipulation of E. coli to produce human insulin. Modified E. coli have been used in vaccine development, bioremediation, and production of immobilised enzymes. E. coli cannot, however, be used to produce some of the more large, complex proteins which contain multiple disulfide bonds and, in particular, unpaired thiols, or proteins that also require post-translational modification for activity.^[49][51][52]

E. coli is frequently used as a model organism in microbiology studies. Cultivated strains (e.g. E. coli K12) are well-adapted to the laboratory environment, and, unlike wild type strains, have lost their ability to thrive in the intestine. Many lab strains lose their ability to form biofilms.^[53][54] These features protect wild type strains from antibodies and other chemical attacks, but require a large expenditure of energy and material resources.

In 1946, Joshua Lederberg and Edward Tatum first described the phenomenon known as bacterial conjugation using E. coli as a model bacterium,^[55] and it remains the primary model to study conjugation. E. coli was an integral part of the first experiments to understand phage genetics,^[56] and early researchers, such as Seymour Benzer, used E. coli and phage T4 to understand the topography of gene structure.^[57] Prior to Benzer’s research, it was not known whether the gene was a linear structure, or if it had a branching pattern.

• Bacterial water analysis
• Coliform bacteria
• Contamination control
• Food poisoning

• E.coli Food poisoning can be long-term problem – Yahoo News
• E. coli statistics
• Spinach and E. coli Outbreak – U.S. FDA
• E. coli Outbreak From Fresh Spinach – U.S. CDC

• EcoCyc: Encyclopedia of E. coli genes and metabolism
• Uropathogenic Escherichia coli (UPEC)
• Genome information on diarrheagenic E.coli and evolutionarily related organisms is available from the NIAID Enteropathogen Resource Integration Center (ERIC)
• EcoliHub
• The community annotation system for E. coli K-12 and its phages and plamids can be found at EcoliWiki
• The structure of the O-antigens that form the basis of the serological classification of E. coli

ECODAB

Template:Model Organisms

an:Escherichia coli bg:Escherichia coli ca:Escheríchia coli cs:Escherichia coli da:Escherichia coli de:Escherichia coli et:Soolekepike hr:Escherichia coli id:Escherichia coli it:Escherichia coli he:Escherichia coli kn:ಎಸ್ಚರೀಶಿಯ ಕೋಲಿ nl:Escherichia coli no:Escherichia coli nn:Escherichia coli oc:Escherichia coli simple:Escherichia coli sl:Escherichia coli sr:Ешерихија коли fi:Escherichia coli sv:Escherichia coli th:อีโคไล chr:Escherichia coli uk:Кишкова паличка

Template:WikiDoc Sources

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Serge Korjian M.D., Yazan Daaboul, M.D.

E. coli enteritis must be differentiated from other causes of abdominal pain, diarrhea, and fever (less common), such as other infectious causes of gastroenteritis, including bacterial, viral, fungal, and parasitic pathogens, in addition to non-infectious causes, including acute pancreatitis, appendicitis, bowel obstruction, diverticulitis, drug reaction, hyperthyroidism, inflammatory bowel disease, mesenteric ischemia, peritonitis, and pneumonia.

• Enteritis caused by E. coli must be differentiated from other causes of acute diarrhea (with or without blood), abdominal pain, and fever (less common).
• Differential diagnosis of E. coli enteritis includes the following:

The following are the infectious differential diagnoses of E. coli enteritis. Common infectious differential diagnoses and differentiating features are shown in the table below.

• Other bacterial infections
• Viral infections (e.g. norovirus infection, HIV infection)
• Fungal infections (e.g. Candida spp.)
• Parasites (Giardia spp., E. histolytica, Cryptosporidium spp.)

The following are the non-infectious differential diagnoses of E. coli enteritis:

• Acute pancreatitis
• Adrenal insufficiency and Waterhouse-Friedrichsen syndrome
• Allergy (e.g. insect bite allergy or anaphylaxis)
• Appendicitis
• Bowel obstruction
• Celiac disease
• Diverticulitis
• Drug reaction (e.g. antimicrobial agents, antihypertensive therapy, chemotherapy, anticonvulsants)
• Endometriosis
• Familial Mediterranean fever
• Gastrointestinal perforation
• Hyperthyroidism
• Ileus
• Inflammatory bowel disease (Crohn’s disease or ulcerative colitis)
• Intussusception
• Ischemic colitis
• Ketoacidosis
• Lactose intolerance
• Lymphoma
• Mesenteric ischemia
• Necrotizing enterocolitis
• Ogilvie syndrome
• Peritonitis
• Pneumonia
• Poisoning and toxicity (e.g. carbon monoxide poisoning, organophosphate poisoning, digitoxin toxicity)
• Ruptured abdominal aortic aneurysm
• Spider bite
• Tropical sprue
• Volvulus
• Urinary tract infection
• Whipple disease

To view a comprehensive list of abdominal pain differential diagnoses, click here.
To view a comprehensive list of diarrhea differential diagnoses, click here.

The table below lists the underlying bacterial pathogens known to cause acute diarrhea:^[1][2]

Escherichia coli enteritis must be differentiated from other causes of viral, bacterial, and parasitic gastroenteritis.

8Small bowel diarrhea: watery, voluminous with less than 5 WBC/high power field

Large bowel diarrhea: Mucousy and/or bloody with less volume and more than 10 WBC/high power field
† It could be as high as 1000 based on patient’s immunity system.

The table below summarizes the findings that differentiate inflammatory causes of chronic diarrhea^{[3][4][5][6][6]}

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Serge Korjian M.D., Yazan Daaboul, M.D.

E. coli is one of the most common causes of diarrhea worldwide and is responsible for 20% to 50% of all infectious diarrhea. The exact incidence of E. coli enteritis is difficult to estimate, but it is thought that E. coli causes more than 500-700 million cases of enteritis and is responsible for approximately 700,000 deaths each year. In the USA, the incidence of E. coli enteritis is estimated to be approximately 20-30 cases per 100,000 individuals. Young children < 5 years of age and elderly individuals are more commonly affected with E. coli enteritis. There is no gender or racial predilection to the development of E. coli enteritis. E. coli enteritis is more common in developing countries than in developed countries.

• E. coli is one of the most common causes of diarrhea worldwide and is responsible for 20% to 50% of all infectious diarrhea.^[1][2][3]
• The exact incidence of E. coli enteritis is difficult to estimate, but it is thought that more than 500-700 million individuals develop E. coli enteritis each year.^[4]

• E. coli enteritis is thought to cause approximately 700,000 deaths worldwide, most of whom are young children < 5 years of age.

• Children and elderly individuals are more commonly affected with E. coli enteritis and are at increased risk of death compared with young and middle-aged adults.^[4]

• There is no gender predilection to the development of E. coli enteritis.

• There is no racial predilection to the development of E. coli enteritis.

• In the USA, the incidence of E. coli enteritis is approximately 20-30 cases per 100,000 individuals.^[4]

• E. coli enteritis is thought to be much more common in developing countries than developed countries due to poor sanitation.^[4]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Serge Korjian M.D., Yazan Daaboul, M.D.

Risk factors in the development of E. coli enteritis include young and old age, immunocompromised status, pregnancy, recent ingestion of uncooked or poorly handled vegetables, meat (e.g. hamburgers), poultry, raw milk, or poorly stored foods that require refrigeration (e.g. mayonnaise), drinking from untreated water, recent travel to developing countries, exposure to infected individuals, daycare, and healthcare settings, and recent sexual history of receptive anal or oral–anal contact.

Risk factors in the development of E. coli enteritis include the following:

• Young age (children < 5 years) or old age
• Immunocompromised status
• Pregnancy
• Recent ingestion of uncooked or poorly handled vegetables, meat, poultry, raw milk, or poorly stored foods that require refrigeration (e.g. mayonnaise)

• Enterohemorrhagic E. coli O157:H7 is commonly associated with ingestion of ground beef (e.g. in hamburgers) or alfalfa sprouts

• Recent drinking from untreated water (e.g. stream or well)
• Recent travel to developing countries

• Enterotoxigenic E. coli is the most common cause of traveler’s diarrhea

• Exposure to daycare
• Exposure to healthcare settings (e.g. nursing homes or hospitals)
• Exposure to infected individuals
• Recent sexual history of receptive anal or oral–anal contact

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Serge Korjian M.D., Yazan Daaboul, M.D.

Screening asymptomatic individuals for the presence of enteritis-causing E. coli strains is not recommended.

Screening asymptomatic individuals for the presence of enteritis-causing E. coli strains is not recommended.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Serge Korjian M.D., Yazan Daaboul, M.D.

Following transmission, the incubation period of pathogenic E. coli strains is approximately 1-10 days, during which the infected patient remains asymptomatic. Early manifestations of E. coli enteritis include diffuse abdominal pain, vomiting, and severe acute watery diarrhea, which may be followed by episodes of bloody diarrhea (in EHEC and EIEC infections). The majority of patients report resolution of symptoms within 5-10 days of symptom-onset. Common complications of E. coli enteritis include hemolytic uremic syndrome (in EHEC infection), thrombotic thrombocytopenic purpura (in EHEC infection), and acute kidney injury. Prognosis of E. coli enteritis is generally excellent, and the majority of cases resolve without any long-term sequelae.

• Following transmission, the incubation period of pathogenic E. coli strains is approximately 1-10 days, during which the infected patient remains asymptomatic.^[1]
• Early manifestations of E. coli enteritis include severe acute watery diarrhea, diffuse abdominal pain, vomiting, with or without fever.
• When infected with either EHEC or EIEC, diarrhea usually converts from watery to bloody as the infection progresses.
• Patients typically report symptoms of dehydration due to excessive diarrhea and vomiting.
• The majority of patients report resolution of symptoms within 5-10 days of symptom-onset.
• In rare cases of EHEC infection, hemolytic uremic syndrome may develop approximately 7 days following the onset of symptoms.

Complications of E. coli enteritis include:^[1]

• Hemolytic uremic syndrome (typically develops in EHEC enteritis)
• Thrombotic thrombocytopenic purpura (TTP)
• Acute kidney injury may be present in severe dehydration

• The prognosis is generally excellent, and the majority of cases resolve without any long-term sequelae.^[1]
• In a minority of cases, patients may die from severe dehydration (more common in developing countries) or severe complications.
• Poor prognostic factors include:

• Young age < 5 years of age
• Old age
• Immunocompromised status
• Pregnancy