| Escherichia coli O157:H7 | |
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| Topographical images of colonies ofE. coli O157:H7 strains (A) 43895OW (curli non-producing) and (B) 43895OR (curli producing) grown on agar for 48 h at 28°C | |
| Specialty | Infectious disease |
Escherichia coli O157:H7 is aserotype of the bacterial speciesEscherichia coli and is one of theShiga-like toxin–producing types ofE. coli. It is a cause ofdisease, typicallyfoodborne illness, through consumption of contaminated and raw food, includingraw milk and undercookedground beef.[1][2] Infection with this type ofpathogenic bacteria may lead to hemorrhagicdiarrhea, and tokidney failure; these have been reported to cause the deaths of children younger than five years of age, of elderly patients, and of patients whose immune systems are otherwise compromised.
Transmission is via thefecal–oral route, and most illness has been through distribution of contaminated raw leaf green vegetables, undercooked meat and raw milk.[3]
E. coli O157:H7 infection often causes severe, acute hemorrhagic diarrhea (although nonhemorrhagic diarrhea is also possible) and abdominalcramps. Usually little or nofever is present, and the illness resolves in 5 to 10 days.[4] It can also sometimes beasymptomatic.[5]
In some people, particularly children under five years of age, persons whose immunologies are otherwise compromised, and the elderly, the infection can causehemolytic–uremic syndrome (HUS), in which thered 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 ofacute kidney failure in children, and most cases of HUS are caused byE. coli O157:H7.[citation needed]
Like the other strains of theE. coli, O157:H7 isgram-negative andoxidase-negative. Unlike many other strains, it does not fermentsorbitol, whichprovides a basis for clinical laboratory differentiation of the strain.Strains ofE. coli that express Shiga and Shiga-like toxins gained that ability viainfection with a prophage containing the structural gene coding for the toxin, and nonproducing strains may become infected and produce shiga-like toxins after incubation with shiga toxin positive strains. Theprophage 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).[6][7]
All clinical isolates ofE. coli O157:H7 possess theplasmidpO157.[8] The periplasmiccatalase is encoded on pO157 and may enhance the virulence of the bacterium by providing additional oxidative protection when infecting the host.[9]E. coli O157:H7 non-hemorrhagic strains are converted to hemorrhagic strains by lysogenic conversion after bacteriophage infection of non-hemorrhagic cells.[citation needed]
While it is relatively uncommon, theE. coli serotype O157:H7 can naturally be found in the intestinal contents of some cattle, goats, and even sheep.[citation needed] The digestive tract of cattle lack the Shiga toxin receptorglobotriaosylceramide, and thus, these can be asymptomatic carriers of the bacterium.[10] The prevalence ofE. coli O157:H7 in North Americanfeedlot cattle herds ranges from 0 to 60%.[11]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 allE. coli O157:H7 excreted.[12]
Infection withE. coli O157:H7 can come from ingestion of contaminated food or water, or oral contact with contaminated surfaces. Examples of this can be undercooked ground beef but also leafy vegetables and raw milk. Fields often become contaminated with the bacterium through irrigation processes or contaminated water naturally entering the soil.[13] It is highlyvirulent, with a lowinfectious dose: an inoculation of fewer than 10 to 100colony-forming units (CFU) ofE. coli O157:H7 is sufficient to cause infection, compared to over a million CFU for other pathogenicE. coli strains.[14]
Astool culture can detect the bacterium. The sample is cultured onsorbitol-MacConkey (SMAC)agar, or the variant cefixime potassium tellurite sorbitol-MacConkey agar (CT-SMAC[15]). On SMAC agar, O157:H7 colonies appear clear due to their inability to ferment sorbitol, while the colonies of the usual sorbitol-fermenting serotypes ofE. coli appear red. Sorbitol non-fermenting colonies are tested for the somatic O157 antigen before being confirmed asE. coli O157:H7. Like all cultures, diagnosis is time-consuming with this method; swifter diagnosis is possible using quickE. coli DNA extraction method[16] pluspolymerase chain reaction techniques. Newer technologies usingfluorescent andantibody detection are also under development.[citation needed]
Avoiding the consumption of, or contact with, unpasteurized dairy products, undercooked beef, uncleaned vegetables, and non disinfected water reduces the risk of anE. coli infection. Properhand washing with water that has been treated with adequate levels of chlorine or other effective disinfectants after using the lavatory or changing a diaper, especially among children or those with diarrhea, reduces the risk of transmission.[17][18]
E. coli O157:H7 infection is a nationallyreportable disease in the US, Great Britain, and Germany. It is also reportable in most states of Australia including Queensland.[19]
While fluid replacement and blood pressure support may be necessary to prevent death from dehydration, most patients recover without treatment in 5–10 days. There is no evidence that antibiotics improve the course of disease, and treatment withantibiotics may precipitatehemolytic–uremic syndrome (HUS).[20] The antibiotics are thought to trigger prophage induction, and the prophages released by the dying bacteria infect other susceptible bacteria, converting them into toxin-producing forms. Antidiarrheal agents, such asloperamide (imodium), should also be avoided as they may prolong the duration of the infection.[citation needed]
Certain novel treatment strategies, such as the use of anti-induction strategies to prevent toxin production[21] and the use of anti-Shiga toxin antibodies,[22] have also been proposed.
The common ancestor of Escherichia coli O157:H7 was found to have originated in the Netherlands around 1890 as estimated by molecular biologists. It is thought that international spread was through animal movements, likeHolstein Friesian cattle.[23] E.coli O157:H7 is thought to have moved from Europe to Australia around 1937, to the United States in 1941, to Canada in 1960, and from Australia to New Zealand in 1966.[23]
The first recorded observation of humanE. coli O157:H7 infection was in 1975, in association with a sporadic case ofhemorrhagic colitis, but it was not identified as pathogenic then.[24] It was first recognized as a human pathogen following a 1982 hemorrhagic colitis outbreak inOregon andMichigan, in which at least 47 people were sickened by eating beef hamburger patties from a fast food chain that were found to be contaminated with it.[25][26][24]
TheUnited States Department of Agriculture banned the sale of ground beef contaminated with the O157:H7 strain in 1994.[27]
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.[28]
In 1982, E. coli O157:H7 was initially identified as the cause of bloody diarrhea from eating undercooked or raw hamburger meat that was contaminated with the bacteria.
E. coli O157:H7 was first described as a cause of human illness and associated with undercooked ground beef in 1982 (1).
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