| Escherichia coli O157:H7 |
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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.
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| Classification and external resources |
| Specialty |
Infectious disease |
| ICD-10 |
A04.3 |
| ICD-9-CM |
008.04 |
Escherichia coli O157:H7 is an enterohemorrhagic serotype of the bacterium Escherichia coli and a cause of illness, typically through consumption of contaminated food.[1] Infection may lead to hemorrhagic diarrhea, and to kidney failure.
Transmission is via the fecal-oral route, and most illness has been through distribution of contaminated raw leaf green vegetables and undercooked meat.[2]
Contents
- 1 Signs and symptoms
- 2 Bacteriology
- 3 Natural habitat
- 4 Transmission
- 5 Diagnosis
- 6 Surveillance
- 7 Treatment
- 8 Costs
- 9 Prevention
- 10 United States
- 11 See also
- 12 References
- 13 External links
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.[citation needed]
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.
Bacteriology
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).[3][4]
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.,[5] E.coli O157:H7 non-hemorrhagic strains are converted to hemorrhagic strains by Lysogenic conversion after a bacteriophage infection to non-hemorrhagic cells.
Natural habitat
While relatively uncommon, E. coli O157:H7 can naturally be found in the intestinal contents of some cattle.[6] Cattle lack the shiga toxin receptor, Globotriaosylceramide, and therefore can be asymptomatic carriers of the bacterium.[7] The prevalence of E. coli O157:H7 in North American feedlot cattle herds ranges from 0 to 60%.[8] 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.[9]
Transmission
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.[10]
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 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[11] plus 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 US states. It is also reportable in most states of Australia including Queensland.
Treatment
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.[12] Antidiarrheal agents, such as loperamide (imodium), should also be avoided as they may prolong the duration of the infection.
Certain novel treatment strategies, such as the use of anti-induction strategies to prevent toxin production[13] and the use of anti-Shiga toxin antibodies,[14] have also been proposed.
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 followup.
Prevention
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.
United States
The U.S.D.A. banned the sale of ground beef contaminated with the O157:H7 strain in 1994.[15]
See also
- 1993 Jack in the Box E. coli outbreak
- 2011 Germany E. coli O104:H4 outbreak
- Escherichia coli O104:H4
- Escherichia coli O121
- Food-induced purpura
- List of foodborne illness outbreaks
- Walkerton E. coli outbreak
- Verotoxin-producing Escherichia coli
References
- ^ Karch H, Tarr P, Bielaszewska M (2005). "Enterohaemorrhagic Escherichia coli in human medicine.". Int J Med Microbiol 295 (6–7): 405–18. doi:10.1016/j.ijmm.2005.06.009. PMID 16238016.
- ^ http://www.cdc.gov/ecoli/outbreaks.html
- ^ O'Brien AD, Newland JW, Miller SF, Holmes RK, Smith HW, Formal SB (November 1984). "Shiga-like toxin-converting phages from Escherichia coli strains that cause hemorrhagic colitis or infantile diarrhea". Science 226 (4675): 694–6. doi:10.1126/science.6387911. PMID 6387911.
- ^ Strockbine NA, Marques LR, Newland JW, Smith HW, Holmes RK, O'Brien AD (July 1986). "Two toxin-converting phages from Escherichia coli O157:H7 strain 933 encode antigenically distinct toxins with similar biologic activities". Infection and immunity 53 (1): 135–40. PMC 260087. PMID 3522426.
- ^ Brunder W, Schmidt H, Karch H (November 1996). "KatP, a novel catalase-peroxidase encoded by the large plasmid of enterohaemorrhagic Escherichia coli O157:H7". Microbiology (Reading, England) 142 (11): 3305–15. doi:10.1099/13500872-142-11-3305. PMID 8969527.
- ^ "Escherichia coli". Retrieved June 24, 2010.
- ^ Pruimboom-Brees IM, Morgan TW, Ackermann MR, Nystrom ED, Samuel JE, Cornick NA, Moon HW (September 2000). "Cattle lack vascular receptors for Escherichia coli O157:H7 Shiga toxins.". Proc Natl Acad Sci U S A. 97 (19): 10325–9. doi:10.1073/pnas.190329997. PMID 10973498.
- ^ Jeon SJ, Elzo M, Dilorenzo N, Lamb GC, Jeong KC (2013). "Evaluation of Animal Genetic and Physiological Factors That Affect the Prevalence of Escherichia coli O157 in Cattle.". PLOS ONE 8 (2): e55728. doi:10.1371/journal.pone.0055728. PMID 23405204.
- ^ Chase-Topping, M; Gally D; Low C; Matthews L; Woolhouse M (2008). "Super-shedding and the link between human infection and livestock carriage of Escherichia coli O157". Nat Rev Microbiol 6 (12): 904–12. doi:10.1038/nrmicro2029. PMID 19008890.
- ^ J.D. Greig, E.C.D. Todd, C. Bartleson, and B. Michaels. March 25, 2010. "Infective Doses and Pathen Carriage", pp. 19-20, USDA 2010 Food Safety Education Conference.
- ^ Quick E. coli DNA extraction filter paper card
- ^ Walterspiel JN, Ashkenazi S, Morrow AL, Cleary TG (1992). "Effect of subinhibitory concentrations of antibiotics on extracellular Shiga-like toxin I". Infection 20 (1): 25–9. doi:10.1007/BF01704889. PMID 1563808.
- ^ Keen, E. C. (December 2012). "Paradigms of pathogenesis: Targeting the mobile genetic elements of disease". Frontiers in Cellular and Infection Microbiology 2: 161. doi:10.3389/fcimb.2012.00161. PMC 3522046. PMID 23248780.
- ^ doi: 10.1128/CMR.17.4.926-941.2004
- ^ "Ban on E. Coli in Ground Beef Is to Extend to 6 More Strains". New York Times. September 12, 2011. Retrieved 2011-10-08.
After the U.S.D.A. banned the O157 form of E. coli from ground beef in 1994, the meat industry sued to block the move, but the agency prevailed in court.
External links
- Haemolytic Uraemic Syndrome Help (HUSH) - a UK Based Charity for Information and Support
- E. coli: Protecting yourself and your family from a sometimes deadly bacterium
- Escherichia coli O157:H7 genomes and related information at PATRIC, a Bioinformatics Resource Center funded by NIAID
- For more information about reducing your risk of foodborne illness, visit the US Department of Agriculture's Food Safety and Inspection Service website or the Partnership for Food Safety Education
- Cooking Ground Beef Safely
- briandeer.com, report from The Sunday Times on a UK outbreak, May 17, 1998
- CBS5 report on September 2006 outbreak
- Infectious diseases
- Bacterial disease: Proteobacterial G−
- primarily A00–A79, 001–041, 080–109
|
|
| α |
| Rickettsiales |
Rickettsiaceae/
(Rickettsioses) |
| Typhus |
- Rickettsia typhi
- Rickettsia prowazekii
- Epidemic typhus, Brill–Zinsser disease, Flying squirrel typhus
|
|
Spotted
fever |
| Tick-borne |
- Rickettsia rickettsii
- Rocky Mountain spotted fever
- Rickettsia conorii
- Rickettsia japonica
- Rickettsia sibirica
- Rickettsia australis
- Rickettsia honei
- Flinders Island spotted fever
- Rickettsia africae
- Rickettsia parkeri
- Rickettsia aeschlimannii
- Rickettsia aeschlimannii infection
|
|
| Mite-borne |
- Rickettsia akari
- Orientia tsutsugamushi
|
|
| Flea-borne |
|
|
|
|
| Anaplasmataceae |
- Ehrlichiosis: Anaplasma phagocytophilum
- Human granulocytic anaplasmosis, Anaplasmosis
- Ehrlichia chaffeensis
- Human monocytotropic ehrlichiosis
- Ehrlichia ewingii
- Ehrlichiosis ewingii infection
|
|
|
| Rhizobiales |
| Brucellaceae |
|
|
| Bartonellaceae |
- Bartonellosis: Bartonella henselae
- Bartonella quintana
- either henselae or quintana
- Bartonella bacilliformis
- Carrion's disease, Verruga peruana
|
|
|
|
| β |
| Neisseriales |
| M+ |
- Neisseria meningitidis/meningococcus
- Meningococcal disease, Waterhouse–Friderichsen syndrome, Meningococcal septicaemia
|
|
| M- |
- Neisseria gonorrhoeae/gonococcus
|
|
| ungrouped: |
- Eikenella corrodens/Kingella kingae
- Chromobacterium violaceum
- Chromobacteriosis infection
|
|
|
| Burkholderiales |
- Burkholderia pseudomallei
- Burkholderia mallei
- Burkholderia cepacia complex
- Bordetella pertussis/Bordetella parapertussis
|
|
|
| γ |
Enterobacteriales
(OX-) |
| Lac+ |
- Klebsiella pneumoniae
- Rhinoscleroma, Klebsiella pneumonia
- Klebsiella granulomatis
- Klebsiella oxytoca
- Escherichia coli: Enterotoxigenic
- Enteroinvasive
- Enterohemorrhagic
- O157:H7
- O104:H4
- Hemolytic-uremic syndrome
- Enterobacter aerogenes/Enterobacter cloacae
|
|
| Slow/weak |
- Serratia marcescens
- Citrobacter koseri/Citrobacter freundii
|
|
| Lac- |
| H2S+ |
- Salmonella enterica
- Typhoid fever, Paratyphoid fever, Salmonellosis
|
|
| H2S- |
- Shigella dysenteriae/sonnei/flexneri/boydii
- Shigellosis, Bacillary dysentery
- Proteus mirabilis/Proteus vulgaris
- Yersinia pestis
- Yersinia enterocolitica
- Yersinia pseudotuberculosis
- Far East scarlet-like fever
|
|
|
|
| Pasteurellales |
| Haemophilus: |
- H. influenzae
- Haemophilus meningitis
- Brazilian purpuric fever
- H. ducreyi
- H. parainfluenzae
|
|
| Pasteurella multocida |
- Pasteurellosis
- Actinobacillus
|
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| Aggregatibacter actinomycetemcomitans |
|
|
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| Legionellales |
- Legionella pneumophila/Legionella longbeachae
- Coxiella burnetii
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| Thiotrichales |
|
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| Vibrionaceae |
- Vibrio cholerae
- Vibrio vulnificus
- Vibrio parahaemolyticus
- Vibrio alginolyticus
- Plesiomonas shigelloides
|
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| Pseudomonadales |
- Pseudomonas aeruginosa
- Moraxella catarrhalis
- Acinetobacter baumannii
|
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| Xanthomonadaceae |
- Stenotrophomonas maltophilia
|
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| Cardiobacteriaceae |
|
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| Aeromonadales |
- Aeromonas hydrophila/Aeromonas veronii
|
|
|
| ε |
| Campylobacterales |
- Campylobacter jejuni
- Campylobacteriosis, Guillain–Barré syndrome
- Helicobacter pylori
- Peptic ulcer, MALT lymphoma, Gastric cancer
- Helicobacter cinaedi
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|
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Index of bacterial disease
|
|
| Description |
|
|
| Disease |
- Gram-positive firmicutes
- Gram-positive actinobacteria
- Gram-negative proteobacteria
- Gram-negative non-proteobacteria
- Cholera
- Tuberculosis
|
|
| Treatment |
- Antibiotics
- cell wall
- nucleic acid
- mycobacteria
- protein synthesis
- other
- Antibodies
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