Escherichia coli O157:H7
|Escherichia coli O157:H7|
Topographical images of colonies of E. coli O157:H7 strains (A) 43895OW (curli non-producing) and (B) 43895OR (curli producing) grown on agar for 48 h at 28°C.
|Classification and external resources|
Escherichia coli O157:H7 is an enterohemorrhagic serotype of the bacterium Escherichia coli and a cause of illness, typically through consumption of contaminated food. Infection may lead to hemorrhagic diarrhea, and to kidney failure.
Signs and symptoms
E. coli O157:H7 infection often causes severe, acute hemorrhagic diarrhea (although nonhemorrhagic diarrhea is also possible) and abdominal cramps. Usually little or no fever is present, and the illness resolves in five to 10 days. It can also be asymptomatic.
In some people, particularly children under five years of age and the elderly, the infection can cause hemolytic uremic syndrome (HUS), 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, HUS is the principal cause of acute kidney failure in children, and most cases of HUS are caused by E. coli O157:H7.
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 nonproducing strains may become infected and produce shiga-like toxins after incubation with shiga toxin positive strains. The prophage responsible seems to have infected the strain's ancestors fairly recently, as viral particles have been observed to replicate in the host if it is stressed in some way (e.g. antibiotics).
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., E.coli O157:H7 non-hemorrhagic strains are converted to hemorrhagic strains by Lysogenic conversion after a bacteriophage infection to non-hemorrhagic cells.
While relatively uncommon, E. coli O157:H7 can naturally be found in the intestinal contents of some cattle. Cattle lack the shiga toxin receptor, Globotriaosylceramide, and therefore can be asymptomatic carriers of the bacterium. The prevalence of E. coli O157:H7 in North American feedlot cattle herds ranges from 0 to 60%. Some cattle may also be so-called 'super-shedders' of the bacterium. Super-shedders may be defined as cattle exhibiting rectoanal junction colonization and excreting >103 to 4 CFU g−1 feces. Super-shedders have been found to constitute a small proportion of the cattle in a feedlot (<10%) but they may account for >90% of all E. coli O157:H7 excreted.
Infection with E. coli O157:H7 follows ingestion of contaminated food or water, or oral contact with contaminated surfaces. It is highly virulent, with a low infectious dose: an inoculation of fewer than 10 to 100 CFU of E. coli O157:H7 is sufficient to cause infection, compared to over one-million CFU for other pathogenic E. coli strains.
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 cefixime potassium tellurite sorbitol-MacConkey agar (CT-SMAC). On SMAC agar O157 colonies appear clear due to their inability to ferment sorbitol, while the colonies of the usual sorbitol-fermenting serotypes of E. coli appear red. Sorbitol nonfermenting colonies are tested for the somatic O157 antigen before being confirmed as E. coli O157. Like all cultures, diagnosis is time-consuming with this method; swifter diagnosis is possible using quick E. coli DNA extraction method plus PCR techniques. Newer technologies using fluorescent and antibody detection are also under development.
E. coli O157:H7 infection is nationally reportable in the USA and Great Britain, and is reportable in most US states. It is also reportable in most states of Australia including Queensland.
While fluid replacement and blood pressure support may be necessary to prevent death from dehydration, most victims recover without treatment in five to 10 days. There is no evidence that antibiotics improve the course of disease, and treatment with antibiotics may precipitate hemolytic uremic syndrome. Antidiarrheal agents, such as loperamide (imodium), should also be avoided as they may prolong the duration of the infection.
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 followup.
Proper hand washing after using the lavatory or changing a diaper, especially among children or those with diarrhea, reduces the risk of transmission. Anyone with a diarrheal illness should avoid swimming in public pools or lakes, sharing baths with others, and preparing food for others.
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- Haemolytic Uraemic Syndrome Help (HUSH) - a UK Based Charity for Information and Support
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