Welcome to Biocare Diagnostics Ltd.
Professional IVD Manufacturer
Supply high sensitivity and specificity
Quality diagnostics reagents at reasonable price
EHEC Rapid Test
Escherichia coli O157:H7 is an
enterohemorrhagic strain of the bacterium Escherichia coli and a cause
of foodborne illness.[1] Infection often leads to bloody diarrhea, and
occasionally to kidney failure, especially in young children and
elderly people. Most illness has been associated with eating
undercooked, contaminated ground beef, drinking unpasteurized milk,
swimming in or drinking contaminated water, and eating contaminated
vegetables.
E. coli serotype O157:H7 is a gram-negative rod-shaped bacterium. The letter "O" (not a zero) in the name refers to the somatic antigen number, whereas the "H" refers to the flagella antigen. Other serotypes may cause (usually less severe) illness, but only those with the specific O157:H7 combination are reviewed here. Other bacteria may be classified by "K" or capsular antigens. (The "O" stands for ohne Hauch [Ger. "without breath" or "without film"]; "H" for Hauch; and "K" for Kapsel.[2][3]) This is one of hundreds of serotypes of the bacterium Escherichia coli. While most strains are harmless and normally found in the intestines of mammals, this strain may produce Shiga-like toxins, cause severe illness, and is a member of a class of pathogenic E. coli known as enterohemorrhagic Escherichia coli or EHEC. Sometimes also referred to by their toxin producing capabilities, Verocytotoxin producing E. coli (VTEC) or Shiga-like Toxin producing E. coli (STEC).Tro
E. coli O157:H7 was first recognized as a pathogen as a result of an outbreak of unusual gastrointestinal illness in 1982. The outbreak was traced to contaminated hamburgers, and the illness was similar to other incidents in the United States and Japan. The etiologic agent of the illness was identified as a rare O157:H7 serotype of Escherichia coli in 1983. This serotype had only been isolated once before, from a sick patient in 1975.
E. coli O157:H7 is markedly different from other pathogenic E. coli, as well. In particular, the O157:H7 serotype is negative for invasiveness (sereny test), elaborates no colonization factors (CFA/I or CFA/II), doesn't produce heat stable or heat labile toxins and is non-hemolytic. In addition, E. coli O157:H7 is usually sorbitol negative whereas 93% of all E. coli ferment sorbitol. E. coli O157:H7 also lacks the ability to hydrolyze 4-methylumbelliferyl-β-D-glucuronide (MUG) and does not grow at 45 °C in the presence of 0.15% bile salts. Because of the latter characteristic this serotype cannot be isolated by using standard fecal coliform methods that include incubation at 45 °C.
E. coli O157:H7 serotypes are closely related, descended from a common ancestor, divergent in plasmid content more than chromosomal content, and are no more related to other shiga toxin producing strains than any other randomly chosen E. coli serotype. E. coli O55:H7 and E. coli O157:H7 are most closely related and diverged from a common pathogenic ancestor that possessed the ability to form attaching and effacing lesions. E. coli O157:H7 serotypes apparently arose as a result of horizontal gene transfer of virulence factors.[8]
Among these virulence factors are a periplasmic catalase and shiga-like toxins. Shiga-like toxins are iron regulated toxins that catalytically inactivate 60S ribosomal subunits of eukaryotic cells blocking mRNA translation and causing cell death.[9] Shiga-like toxins are functionally identical to toxins produced by virulent Shigella species.[10] Strains of E. coli that express shiga-like toxins gained this ability due to infection with a prophage containing the structural coding for the toxin, and non-producing strains may become infected and produce shiga-like toxins after incubation with shiga toxin positive strains.[11][12] The periplasmic catalase is encoded on the pO157 plasmid and is believed to be involved in virulence by providing additional oxidative protection when infecting the host
Transmission
A major source of infection is undercooked ground beef; other sources include consumption of unpasteurized milk and juice, raw sprouts, lettuce, and salami, and contact with infected live animals. Disease caused by E.coli O157:H7 is known as the "hamburger disease" because of its association with eating home-made hamburgers. Association with hamburgers from commercial fast food chains has become rare as the chains now use cooking procedures designed to destroy the bacteria.
Waterborne transmission occurs through swimming in contaminated lakes, pools, or drinking inadequately treated water. The organism is easily transmitted from person to person and has been difficult to control in child day-care centers.
E.coli O157:H7 is found on cattle farms and can live in the intestines of healthy cattle. The toxin requires highly specific receptors on the cells' surface in order to attach and enter the cell; species such as cattle, swine, and deer which do not carry these receptors may harbor toxigenic bacteria without any ill effect, shedding them in their feces from which they may be spread to humans. Meat can become contaminated during slaughter, and organisms can be thoroughly mixed into beef when it is ground into hamburger. Bacteria present on the cow's udders or on equipment may get into raw milk. Although the number of organisms required to cause disease is not known, it is suspected to be very small.
Eating contaminated meat (especially ground meat) or produce that has not been cooked sufficiently to kill E. coli O157:H7 can cause infection. Contaminated foods look, smell and taste normal.
Signs and symptoms
E. coli O157:H7 infection often causes severe, acute bloody diarrhoea (although non-bloody diarrhoea is also possible) and abdominal cramps. Usually little or no fever is present, and the illness resolves in 5 to 10 days. It can also be asymptomatic.
In some people, particularly children under 5 years of age and the elderly, the infection can cause haemolytic 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, haemolytic uremic syndrome is the principal cause of acute kidney failure in children, and most cases of haemolytic uremic syndrome are caused by E. coli O157:H7.
Diagnosis
A stool culture can detect the bacterium, although it is not a routine test and so must be specifically requested. The sample is cultured on sorbitol-MacConkey (SMAC) agar, or the variant cefeximine potassium tellurite sorbitol-MacConkey agar (CT-SMAC). On SMAC agar O157 colonies appear colourless due to their inability (unlike other E. coli serotypes) to ferment sorbitol. Non-sorbitol fermenting colonies are tested for the somatic O157 antigen before being confirmed as E coli O157. Like all cultures, diagnosis is slow using this method, and more rapid diagnosis is possible using PCR techniques. Newer technologies using fluorescent and antibody detection are also under development.
Surveillance
E. coli O157:H7 infection is nationally reportable in the USA and Great Britain, and is reportable in most U.S. states. HUS (hemolytic-uremic syndrome) is also reportable in most US states.
Treatment
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.[14] Antidiarrheal agents, such as loperamide (imodium), should also be avoided.
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%.
Prognosis
The majority of infections resolve completely. Of those who develop hemolytic uremic syndrome, one third have abnormal kidney function many years later, 3–5% die (causing about 61 deaths annually in the USA), a few require long-term dialysis, and another 8% develop other lifelong complications, such as high blood pressure, seizures, blindness, paralysis, and, if surgery is required to remove part of the bowel, additional procedure-related side-effects.
There are currently long term studies continuing in Walkerton, Ontario, looking at the long term effects of E. coli O157:H7 after approximately 2500 people were infected through the municipal water system in May 2000.
Costs
The pathogen results in an estimated 2,100 hospitalizations annually in the United States. The illness is often misdiagnosed; therefore, expensive and invasive diagnostic procedures may be performed. Patients who develop HUS often require prolonged hospitalization, dialysis, and long-term follow-up.
E. coli serotype O157:H7 is a gram-negative rod-shaped bacterium. The letter "O" (not a zero) in the name refers to the somatic antigen number, whereas the "H" refers to the flagella antigen. Other serotypes may cause (usually less severe) illness, but only those with the specific O157:H7 combination are reviewed here. Other bacteria may be classified by "K" or capsular antigens. (The "O" stands for ohne Hauch [Ger. "without breath" or "without film"]; "H" for Hauch; and "K" for Kapsel.[2][3]) This is one of hundreds of serotypes of the bacterium Escherichia coli. While most strains are harmless and normally found in the intestines of mammals, this strain may produce Shiga-like toxins, cause severe illness, and is a member of a class of pathogenic E. coli known as enterohemorrhagic Escherichia coli or EHEC. Sometimes also referred to by their toxin producing capabilities, Verocytotoxin producing E. coli (VTEC) or Shiga-like Toxin producing E. coli (STEC).Tro
E. coli O157:H7 was first recognized as a pathogen as a result of an outbreak of unusual gastrointestinal illness in 1982. The outbreak was traced to contaminated hamburgers, and the illness was similar to other incidents in the United States and Japan. The etiologic agent of the illness was identified as a rare O157:H7 serotype of Escherichia coli in 1983. This serotype had only been isolated once before, from a sick patient in 1975.
E. coli O157:H7 is markedly different from other pathogenic E. coli, as well. In particular, the O157:H7 serotype is negative for invasiveness (sereny test), elaborates no colonization factors (CFA/I or CFA/II), doesn't produce heat stable or heat labile toxins and is non-hemolytic. In addition, E. coli O157:H7 is usually sorbitol negative whereas 93% of all E. coli ferment sorbitol. E. coli O157:H7 also lacks the ability to hydrolyze 4-methylumbelliferyl-β-D-glucuronide (MUG) and does not grow at 45 °C in the presence of 0.15% bile salts. Because of the latter characteristic this serotype cannot be isolated by using standard fecal coliform methods that include incubation at 45 °C.
E. coli O157:H7 serotypes are closely related, descended from a common ancestor, divergent in plasmid content more than chromosomal content, and are no more related to other shiga toxin producing strains than any other randomly chosen E. coli serotype. E. coli O55:H7 and E. coli O157:H7 are most closely related and diverged from a common pathogenic ancestor that possessed the ability to form attaching and effacing lesions. E. coli O157:H7 serotypes apparently arose as a result of horizontal gene transfer of virulence factors.[8]
Among these virulence factors are a periplasmic catalase and shiga-like toxins. Shiga-like toxins are iron regulated toxins that catalytically inactivate 60S ribosomal subunits of eukaryotic cells blocking mRNA translation and causing cell death.[9] Shiga-like toxins are functionally identical to toxins produced by virulent Shigella species.[10] Strains of E. coli that express shiga-like toxins gained this ability due to infection with a prophage containing the structural coding for the toxin, and non-producing strains may become infected and produce shiga-like toxins after incubation with shiga toxin positive strains.[11][12] The periplasmic catalase is encoded on the pO157 plasmid and is believed to be involved in virulence by providing additional oxidative protection when infecting the host
Transmission
A major source of infection is undercooked ground beef; other sources include consumption of unpasteurized milk and juice, raw sprouts, lettuce, and salami, and contact with infected live animals. Disease caused by E.coli O157:H7 is known as the "hamburger disease" because of its association with eating home-made hamburgers. Association with hamburgers from commercial fast food chains has become rare as the chains now use cooking procedures designed to destroy the bacteria.
Waterborne transmission occurs through swimming in contaminated lakes, pools, or drinking inadequately treated water. The organism is easily transmitted from person to person and has been difficult to control in child day-care centers.
E.coli O157:H7 is found on cattle farms and can live in the intestines of healthy cattle. The toxin requires highly specific receptors on the cells' surface in order to attach and enter the cell; species such as cattle, swine, and deer which do not carry these receptors may harbor toxigenic bacteria without any ill effect, shedding them in their feces from which they may be spread to humans. Meat can become contaminated during slaughter, and organisms can be thoroughly mixed into beef when it is ground into hamburger. Bacteria present on the cow's udders or on equipment may get into raw milk. Although the number of organisms required to cause disease is not known, it is suspected to be very small.
Eating contaminated meat (especially ground meat) or produce that has not been cooked sufficiently to kill E. coli O157:H7 can cause infection. Contaminated foods look, smell and taste normal.
Signs and symptoms
E. coli O157:H7 infection often causes severe, acute bloody diarrhoea (although non-bloody diarrhoea is also possible) and abdominal cramps. Usually little or no fever is present, and the illness resolves in 5 to 10 days. It can also be asymptomatic.
In some people, particularly children under 5 years of age and the elderly, the infection can cause haemolytic 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, haemolytic uremic syndrome is the principal cause of acute kidney failure in children, and most cases of haemolytic uremic syndrome are caused by E. coli O157:H7.
Diagnosis
A stool culture can detect the bacterium, although it is not a routine test and so must be specifically requested. The sample is cultured on sorbitol-MacConkey (SMAC) agar, or the variant cefeximine potassium tellurite sorbitol-MacConkey agar (CT-SMAC). On SMAC agar O157 colonies appear colourless due to their inability (unlike other E. coli serotypes) to ferment sorbitol. Non-sorbitol fermenting colonies are tested for the somatic O157 antigen before being confirmed as E coli O157. Like all cultures, diagnosis is slow using this method, and more rapid diagnosis is possible using PCR techniques. Newer technologies using fluorescent and antibody detection are also under development.
Surveillance
E. coli O157:H7 infection is nationally reportable in the USA and Great Britain, and is reportable in most U.S. states. HUS (hemolytic-uremic syndrome) is also reportable in most US states.
Treatment
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.[14] Antidiarrheal agents, such as loperamide (imodium), should also be avoided.
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%.
Prognosis
The majority of infections resolve completely. Of those who develop hemolytic uremic syndrome, one third have abnormal kidney function many years later, 3–5% die (causing about 61 deaths annually in the USA), a few require long-term dialysis, and another 8% develop other lifelong complications, such as high blood pressure, seizures, blindness, paralysis, and, if surgery is required to remove part of the bowel, additional procedure-related side-effects.
There are currently long term studies continuing in Walkerton, Ontario, looking at the long term effects of E. coli O157:H7 after approximately 2500 people were infected through the municipal water system in May 2000.
Costs
The pathogen results in an estimated 2,100 hospitalizations annually in the United States. The illness is often misdiagnosed; therefore, expensive and invasive diagnostic procedures may be performed. Patients who develop HUS often require prolonged hospitalization, dialysis, and long-term follow-up.