Overview

Brief Summary

Gut bacteria are rod-shaped. Many are found the intestines of animals, including humans. Many strains of E. coli normally live in the human large intestine and cause no harm. A few strains, however, can cause serious illness, including severe diarrhea and kidney failure.

Creative Commons Attribution 3.0 (CC BY 3.0)

© Sebastian Velvez

Supplier: Life on Earth

Unreviewed

Article rating from 0 people

Default rating: 2.5 of 5

Evolution and Systematics

Functional Adaptations

Functional adaptation

Colonies grow restraint: Escherichia coli
 

Colonies of Escherichia coli bacteria survive longer by developing restraint that allows competitors to survive.

       
  "New research...shows that in  some structured communities, organisms increase their chances of  survival if they evolve some level of restraint that allows competitors  to survive as well, a sort of 'survival of the weakest.' The phenomenon was observed in a community of three 'nontransitive'  competitors, meaning their relationship to each other is circular as in  the children's game rock-paper-scissors in which scissors always  defeats paper, paper always defeats rock and rock always defeats  scissors...'By becoming a better competitor in a well-mixed system, it could  actually drive itself to extinction,' said Joshua Nahum...The restrained patches, the ones that grew slower, seemed to last  longer and the unrestrained patches, the ones that grew faster, burned  themselves out faster'...To understand the process, imagine a community of three strains [of bacteria],  Rock, Paper and Scissors, and then imagine the emergence of an  unrestrained supercompetitor, Rock* (rock star), that is able to  displace Scissors even faster than regular Rock can. But that also makes  Rock* a better competitor against Rock, the researchers said.  Eventually Rock* will be a victim of its own success, being preyed upon  by Paper." (Stricherz 2011:1)
  Learn more about this functional adaptation.
  • Nahum JR; Harding BN; Kerr B. 2011. Evolution of restraint in a structured rock–paper–scissors community. PNAS. 108(2): 10831-10838.
  • Stricherz V. 2011. Bacteria develop restraint for survival in a rock-paper-scissors community. EurekAlert [Internet], Accessed 20 June 2011.
Creative Commons Attribution Non Commercial 3.0 (CC BY-NC 3.0)

© The Biomimicry Institute

Source: AskNature

Trusted

Article rating from 0 people

Default rating: 2.5 of 5

Functional adaptation

Bacteria sense and move toward chemicals: Escherichia coli
 

The membrane of E. coli bacteria detects chemicals of interest via transmembrane receptor proteins.

   
  "Chemotactic bacteria navigate complex chemical environments by coupling sophisticated information processing capabilities to powerful molecular motors that propel the cells forward. Escherichia coli recognize chemoattractants using five transmembrane receptor proteins, which cluster with one another and interact with a set of well-characterized cytosolic proteins to effect changes in the directional rotation of the flagellar motor." (Topp 2007:6807)
  Learn more about this functional adaptation.
  • Topp, S.; Gallivan, J. P. 2007. Guiding Bacteria with Small Molecules and RNA. J. Am. Chem. Soc.
Creative Commons Attribution Non Commercial 3.0 (CC BY-NC 3.0)

© The Biomimicry Institute

Source: AskNature

Trusted

Article rating from 0 people

Default rating: 2.5 of 5

Wikipedia

Escherichia coli

"E. coli" redirects here. For the protozoan commensal, see Entamoeba coli.
This article is about Escherichia coli as a species. For E. coli in medicine, see Pathogenic Escherichia coli. For E. coli in molecular biology, see Escherichia coli (molecular biology).

Escherichia coli (/ˌɛʃɨˈrɪkiə ˈkl/;[1] commonly abbreviated E. coli) is a Gram-negative, facultatively anaerobic, rod-shaped bacterium of the genus Escherichia that is commonly found in the lower intestine of warm-blooded organisms (endotherms).[2] Most E. coli strains are harmless, but some serotypes can cause serious food poisoning in their hosts, and are occasionally responsible for product recalls due to food contamination.[3][4] The harmless strains are part of the normal flora of the gut, and can benefit their hosts by producing vitamin K2,[5] and preventing colonization of the intestine with pathogenic bacteria.[6][7]

E. coli and other facultative anaerobes constitute about 0.1% of gut flora,[8] and fecal–oral transmission is the major route through which pathogenic strains of the bacterium cause disease. Cells are able to survive outside the body for a limited amount of time, which makes them ideal indicator organisms to test environmental samples for fecal contamination.[9][10] There is, however, a growing body of research that has examined environmentally persistent E. coli which can survive for extended periods outside of the host.[11]

The bacterium can be grown easily and inexpensively in a laboratory setting, and has been intensively investigated for over 60 years. E. coli is the most widely studied prokaryotic model organism, and an important species in the fields of biotechnology and microbiology, where it has served as the host organism for the majority of work with recombinant DNA. Under favourable conditions it takes only 20 minutes to reproduce.[12]

Biology and biochemistry[edit]

Model of successive binary fission in E. coli

E. coli is Gram-negative (bacteria which do not retain Crystal violet dye), facultative anaerobic (that makes ATP by aerobic respiration if oxygen is present, but is capable of switching to fermentation or anaerobic respiration if oxygen is absent) and non-sporulating.[13] Cells are typically rod-shaped, and are about 2.0 micrometers (μm) long and 0.25–1.0 μm in diameter, with a cell volume of 0.6–0.7 μm3.[14][15] 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 sulphate-reducing bacteria.[16]

Optimal growth of E. coli occurs at 37 °C (98.6 °F) but some laboratory strains can multiply at temperatures of up to 49 °C (120 °F).[17] 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, fumarate, dimethyl sulfoxide and trimethylamine N-oxide.[18]

Strains that possess flagella are motile. The flagella have a peritrichous arrangement.[19]

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. This process led to the spread of the gene encoding shiga toxin from Shigella to E. coli O157:H7, carried by a bacteriophage.[20]

Diversity[edit]

Escherichia coli encompasses an enormous population of bacteria that exhibit a very high degree of both genetic and phenotypic diversity. Genome sequencing of a large number of isolates of E. coli and related bacteria shows that a taxonomic reclassification would be desirable. However, this has not been done, largely due to its medical importance[21] and E. coli remains one of the most diverse bacterial species: only 20% of the genome is common to all strains.[22]

In fact, from the evolutionary point of view, the members of genus Shigella (S. dysenteriae, S. flexneri, S. boydii, S. sonnei) should be classified as E. coli strains, a phenomenon termed taxa in disguise.[23] Similarly, other strains of E. coli (e.g. the K-12 strain commonly used in recombinant DNA work) are sufficiently different that they would merit reclassification.

A strain is a sub-group within the species that has unique characteristics that distinguish it from other strains. These differences are often detectable only at the molecular level; however, they may result in changes to the physiology or lifecycle of the bacterium. For example, a strain may gain pathogenic capacity, the ability to use a unique carbon source, the ability to take upon 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.[9][10] For example, knowing which E. coli strains are present in a water sample allows researchers to make assumptions about whether the contamination originated from a human, another mammal or a bird.

Serotypes[edit]

A common subdivision system of E. coli, but not based on evolutionary relatedness, is by serotype, which is based on major surface antigens (O antigen: part of lipopolysaccharide layer; H: flagellin; K antigen: capsule), e.g. O157:H7).[24] It is however common to cite only the serogroup, i.e. the O-antigen. At present about 190 serogroups are known.[25] The common laboratory strain has a mutation that prevents the formation of an O-antigen and is thus non-typeable.

Genome plasticity[edit]

Like all lifeforms, new strains of E. coli evolve through the natural biological processes of mutation, gene duplication and horizontal gene transfer, in particular 18% of the genome of the laboratory strain MG1655 was horizontally acquired since the divergence from Salmonella.[26] E. coli K-12 and E. coli B strains are the most frequently used varieties for laboratory purposes. Some strains develop traits that can be harmful to a host animal. These virulent strains typically cause a bout of diarrhea that is unpleasant in healthy adults and is often lethal to children in the developing world.[27] More virulent strains, such as O157:H7 cause serious illness or death in the elderly, the very young or the immunocompromised.[6][27]

Neotype strain[edit]

E. coli is the type species of the genus (Escherichia) and in turn Escherichia is the type genus of the family Enterobacteriaceae, where it should be noted that the family name does not stem from the genus Enterobacter + "i" (sic.) + "aceae", but from "enterobacterium" + "aceae" (enterobacterium being not a genus, but an alternative trivial name to enteric bacterium).[28][29][30]

The original strain described by Escherich is believed to be lost, consequently a new type strain (neotype) was chosen as a representative: the neotype strain is ATCC 11775,[31] also known as NCTC 9001,[32] which is pathogenic to chickens and has an O1:K1:H7 serotype.[33] However, in most studies either O157:H7 or K-12 MG1655 or K-12 W3110 are used as a representative E.coli.

Phylogeny of Escherichia coli strains[edit]

A large number of strains belonging to this species have been isolated and characterised. In addition to serotype (vide supra), they can be classified according to their phylogeny, i.e. the inferred evolutionary history, as shown below where the species is divided into six groups.[22][34]

The link between phylogenetic distance ("relatedness") and pathology is small, e.g. the O157:H7 serotype strains, which form a clade ("an exclusive group")—group E below—are all enterohaemorragic strains (EHEC), but not all EHEC strains are closely related. In fact, four different species of Shigella are nested among E. coli strains (vide supra), while Escherichia albertii and Escherichia fergusonii are outside of this group. All commonly used research strains of E. coli belong to group A and are derived mainly from Clifton's K-12 strain (λ⁺ F⁺; O16) and to a lesser degree from d'Herelle's Bacillus coli strain (B strain)(O7).



Salmonella enterica




E. albertii




E. fergusonii




Group B2

E. coli SE15 (O150:H5. Commensal)



E. coli E2348/69 (O127:H6. Enteropathogenic)




Group D

E. coli UMN026 (O17:K52:H18. Extracellular pathogenic)




E. coli (O19:H34. Extracellular pathogenic)



E. coli (O7:K1. Extracellular pathogenic)





group E


E. coli EDL933 (O157:H7 EHEC)



E. coli Sakai (O157:H7 EHEC)





E. coli EC4115 (O157:H7 EHEC)



E. coli TW14359 (O157:H7 EHEC)





Shigella


Shigella dysenteriae




Shigella sonnei




Shigella flexneri







Group B1


E. coli E24377A (O139:H28. Enterotoxigenic)






E. coli E110019




E. coli 11368 (O26:H11. EHEC)



E. coli 11128 (O111:H-. EHEC)







E. coli IAI1 O8 (Commensal)



E. coli 53638 (EIEC)





E. coli SE11 (O152:H28. Commensal)



E. coli B7A









E. coli 12009 (O103:H2. EHEC)



E. coli GOS1 (O104:H4 EAHEC) German 2011 outbreak




E. coli E22





E. coli Olso O103



E. coli 55989 (O128:H2. Enteroaggressive)







Group A


E. coli ATCC8739 (O146. Crook's E.coli used in phage work in the 1950s)




K-12 strain derivatives

E. coli K-12 W3110 (O16. λ⁻ F⁻ "wild type" molecular biology strain)



E. coli K-12 DH10b (O16. high electrocompetency molecular biology strain)



E. coli K-12 DH1 (O16. high chemical competency molecular biology strain)



E. coli K-12 MG1655 (O16. λ⁻ F⁻ "wild type" molecular biology strain)



E. coli BW2952 (O16. competent molecular biology strain)





E. coli 101-1 (O? H?. EAEC)


B strain derivatives

E. coli B REL606 (O7. high competency molecular biology strain)



E. coli BL21-DE3 (O7. expression molecular biology strain with T7 polymerase for pET system)














Genomics[edit]

The first complete DNA sequence of an E. coli genome (laboratory strain K-12 derivative MG1655) was published in 1997. It was found to be a circular DNA molecule 4.6 million base pairs in length, containing 4288 annotated protein-coding genes (organized into 2584 operons), seven ribosomal RNA (rRNA) operons, and 86 transfer RNA (tRNA) genes. Despite having been the subject of intensive genetic analysis for approximately 40 years, a large number of these genes were previously unknown. The coding density was found to be very high, with a mean distance between genes of only 118 base pairs. The genome was observed to contain a significant number of transposable genetic elements, repeat elements, cryptic prophages, and bacteriophage remnants.[35]

Today, over 60 complete genomic sequences of Escherichia and Shigella species are available. Comparison of these sequences shows a remarkable amount of diversity; only about 20% of each genome represents sequences present in every one of the isolates, while approximately 80% of each genome can vary among isolates.[22] Each individual genome contains between 4,000 and 5,500 genes, but the total number of different genes among all of the sequenced E. coli strains (the pan-genome) exceeds 16,000. This very large variety of component genes has been interpreted to mean that two-thirds of the E. coli pangenome originated in other species and arrived through the process of horizontal gene transfer.[36]

Proteomics[edit]

Proteome[edit]

Several studies have investigated the proteome of E. coli. By 2006, 1,627 (38%) of the 4,237 open reading frames (ORFs) had been identified experimentally.[37]

Interactome[edit]

The interactome of E. coli has been studied by affinity purification and mass spectrometry (AP/MS) and by analyzing the binary interactions among its proteins.

Protein complexes. A 2006 study purified 4,339 proteins from cultures of strain K-12 and found interacting partners for 2,667 proteins, many of which had unknown functions at the time.[38] A 2009 study found 5,993 interactions between proteins of the same E. coli strain though this data showed little overlap with that of the 2006 publication.[39]

Binary interactions. Rajagopala et al. (2014) have carried out systematic yeast two-hybrid screens with most E. coli proteins and found a total of 2,234 protein-protein interactions.[40] This study also integrated genetic interactions and protein structures and mapped 458 interactions within 227 protein complexes.

Normal microbiota[edit]

E. coli normally colonizes an infant's gastrointestinal tract within 40 hours of birth, arriving with food or water or with the individuals handling the child. In the bowel, it adheres to the mucus of the large intestine. It is the primary facultative anaerobe of the human gastrointestinal tract.[41] (Facultative anaerobes are organisms that can grow in either the presence or absence of oxygen.) As long as these bacteria do not acquire genetic elements encoding for virulence factors, they remain benign commensals.[42]

Therapeutic use[edit]

Nonpathogenic Escherichia coli strain Nissle 1917 also known as Mutaflor and Escherichia coli O83:K24:H31 (known as Colinfant[43]) are used as a probiotic agents in medicine, mainly for the treatment of various gastroenterological diseases,[44] including inflammatory bowel disease.[45]

Role in disease[edit]

Most E. coli strains do not cause disease,[46] but virulent strains can cause gastroenteritis, urinary tract infections, and neonatal meningitis. In rarer cases, virulent strains are also responsible for hemolytic-uremic syndrome, peritonitis, mastitis, septicemia and Gram-negative pneumonia.[41]

UPEC (uropathogenic E. coli) is one of the main causes of urinary tract infections.[47] It is part of the normal flora in the gut and can be introduced in many ways. In particular for females, the direction of wiping after defecation (wiping back to front) can lead to fecal contamination of the urogenital orifices. Anal intercourse can also introduce this bacteria into the male urethra, and in switching from anal to vaginal intercourse the male can also introduce UPEC to the female urogenital system.[47] For more information, see the databases at the end of the article or UPEC pathogenicity.

In May 2011, one E. coli strain, Escherichia coli O104:H4, has been the subject of a bacterial outbreak that began in Germany. Certain strains of E. coli are a major cause of foodborne illness. The outbreak started when several people in Germany were infected with enterohemorrhagic E. coli (EHEC) bacteria, leading to hemolytic-uremic syndrome (HUS), a medical emergency that requires urgent treatment. The outbreak did not only concern Germany, but 11 other countries, including regions in North America.[48] On 30 June 2011 the German Bundesinstitut für Risikobewertung (BfR) (Federal Institute for Risk Assessment, a federal, fully legal entity under public law of the Federal Republic of Germany, an institute within the German Federal Ministry of Food, Agriculture and Consumer Protection) announced that seeds of fenugreek from Egypt were likely the cause of the EHEC outbreak.[49]

Model organism in life science research[edit]

Role in biotechnology[edit]

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.[50] The work of Stanley Norman Cohen and Herbert Boyer in E. coli, using plasmids and restriction enzymes to create recombinant DNA, became a foundation of biotechnology.[51]

E. coli is a very versatile host for the production of heterologous proteins,[52] and various protein expression systems have been developed which allow the production of recombinant proteins in E. coli. Researchers can introduce genes into the microbes using plasmids which permit high level expression of protein, and such protein may be mass-produced in industrial fermentation processes. One of the first useful applications of recombinant DNA technology was the manipulation of E. coli to produce human insulin.[53]

Many proteins previously thought difficult or impossible to be expressed in E. coli in folded form have also been successfully expressed in E. coli. For example, proteins with multiple disulphide bonds may be produced in the periplasmic space or in the cytoplasm of mutants rendered sufficiently oxidizing to allow disulphide-bonds to form,[54] while proteins requiring post-translational modification such as glycosylation for stability or function have been expressed using the N-linked glycosylation system of Campylobacter jejuni engineered into E. coli.[55][56][57]

Modified E. coli cells have been used in vaccine development, bioremediation, production of biofuels;[58] lighting, and production of immobilised enzymes.[52][59]

Model organism[edit]

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.[60][61] 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,[62] and it remains the primary model to study conjugation.[63] E. coli was an integral part of the first experiments to understand phage genetics,[64] and early researchers, such as Seymour Benzer, used E. coli and phage T4 to understand the topography of gene structure.[65] Prior to Benzer's research, it was not known whether the gene was a linear structure, or if it had a branching pattern.[66]

E. coli was one of the first organisms to have its genome sequenced; the complete genome of E. coli K12 was published by Science in 1997.[35]

The long-term evolution experiments using E. coli, begun by Richard Lenski in 1988, have allowed direct observation of major evolutionary shifts in the laboratory.[67] In this experiment, one population of E. coli unexpectedly evolved the ability to aerobically metabolize citrate, which is extremely rare in E. coli. As the inability to grow aerobically is normally used as a diagnostic criterion with which to differentiate E. coli from other, closely related bacteria, such as Salmonella, this innovation may mark a speciation event observed in the lab.

By evaluating the possible combination of nanotechnologies with landscape ecology, complex habitat landscapes can be generated with details at the nanoscale.[68] On such synthetic ecosystems, evolutionary experiments with E. coli have been performed to study the spatial biophysics of adaptation in an island biogeography on-chip.

Studies are also being performed attempting to program E. coli to solve complicated mathematics problems, such as the Hamiltonian path problem.[69]

History[edit]

The genera Escherichia and Salmonella diverged around 102 million years ago (credibility interval: 57–176 mya), which coincides with the divergence of their hosts: the former being found in mammals and the latter in birds and reptiles.[70] This was followed by a split of the escherichian ancestor into five species (E. albertii, E. coli, E. fergusonii, E. hermannii and E. vulneris.) The last E. coli ancestor split between 20 and 30 million years ago.[71]

In 1885, the German-Austrian pediatrician Theodor Escherich, discovered this organism in the feces of healthy individuals and called it Bacterium coli commune due to the fact it is found in the colon and early classifications of Prokaryotes placed these in a handful of genera based on their shape and motility (at that time Ernst Haeckel's classification of Bacteria in the kingdom Monera was in place[72]).[73] Bacterium coli was the type species of the now invalid genus Bacterium when it was revealed that the former type species ("Bacterium triloculare") was missing.[74] Following a revision of Bacterium it was reclassified as Bacillus coli by Migula in 1895[75] and later reclassified in the newly created genus Escherichia, named after its original discoverer.[76]

The genus belongs in a group of bacteria informally known as "coliforms", and is a member of the Enterobacteriaceae family ("the enterics") of the Gammaproteobacteria.[28]

See also[edit]

References[edit]

  1. ^ "coli". Oxford English Dictionary (3rd ed.). Oxford University Press. September 2005. 
  2. ^ Singleton P (1999). Bacteria in Biology, Biotechnology and Medicine (5th ed.). Wiley. pp. 444–454. ISBN 0-471-98880-4. 
  3. ^ "Escherichia coli". CDC National Center for Emerging and Zoonotic Infectious Diseases. Retrieved 2012-10-02. 
  4. ^ Vogt RL, Dippold L (2005). "Escherichia coli O157:H7 outbreak associated with consumption of ground beef, June–July 2002". Public Health Rep 120 (2): 174–8. PMC 1497708. PMID 15842119. 
  5. ^ Bentley R, Meganathan R (1 September 1982). "Biosynthesis of vitamin K (menaquinone) in bacteria". Microbiol. Rev. 46 (3): 241–80. PMC 281544. PMID 6127606. 
  6. ^ a b Hudault S, Guignot J, Servin AL (July 2001). "Escherichia coli strains colonizing the gastrointestinal tract protect germ-free mice against Salmonella typhimurium infection". Gut 49 (1): 47–55. doi:10.1136/gut.49.1.47. PMC 1728375. PMID 11413110. 
  7. ^ Reid G, Howard J, Gan BS (September 2001). "Can bacterial interference prevent infection?". Trends Microbiol. 9 (9): 424–428. doi:10.1016/S0966-842X(01)02132-1. PMID 11553454. 
  8. ^ Eckburg PB, Bik EM, Bernstein CN, Purdom E, Dethlefsen L, Sargent M, Gill SR, Nelson KE, Relman DA (June 2005). "Diversity of the human intestinal microbial flora". Science 308 (5728): 1635–8. Bibcode:2005Sci...308.1635E. doi:10.1126/science.1110591. PMC 1395357. PMID 15831718. 
  9. ^ a b Feng P, Weagant S, Grant, M (2002-09-01). "Enumeration of Escherichia coli and the Coliform Bacteria". Bacteriological Analytical Manual (8th ed.). FDA/Center for Food Safety & Applied Nutrition. Retrieved 2007-01-25. 
  10. ^ a b Thompson, Andrea (2007-06-04). "E. coli Thrives in Beach Sands". Live Science. Retrieved 2007-12-03. 
  11. ^ Ishii S, Sadowsky MJ (2008). "Escherichia coli in the Environment: Implications for Water Quality and Human Health". Microbes Environ. 23 (2): 101–8. doi:10.1264/jsme2.23.101. PMID 21558695. 
  12. ^ "Bacteria". Microbiologyonline. Retrieved 27 February 2014. 
  13. ^ "E.Coli". Redorbit. Retrieved 27 November 2013. 
  14. ^ "Facts about E. coli: dimensions, as discussed in bacteria: Diversity of structure of bacteria: – Britannica Online Encyclopedia". Britannica.com. Retrieved 2011-06-05. 
  15. ^ Kubitschek HE (1 January 1990). "Cell volume increase in Escherichia coli after shifts to richer media". J. Bacteriol. 172 (1): 94–101. PMC 208405. PMID 2403552. 
  16. ^ Madigan MT, Martinko JM (2006). Brock Biology of microorganisms (11th ed.). Pearson. ISBN 0-13-196893-9. 
  17. ^ Fotadar U, Zaveloff P, Terracio L (2005). "Growth of Escherichia coli at elevated temperatures". J. Basic Microbiol. 45 (5): 403–4. doi:10.1002/jobm.200410542. PMID 16187264. 
  18. ^ Ingledew WJ, Poole RK (1984). "The respiratory chains of Escherichia coli". Microbiol. Rev. 48 (3): 222–71. PMC 373010. PMID 6387427. 
  19. ^ Darnton NC, Turner L, Rojevsky S, Berg HC (March 2007). "On torque and tumbling in swimming Escherichia coli". J. Bacteriol. 189 (5): 1756–64. doi:10.1128/JB.01501-06. PMC 1855780. PMID 17189361. 
  20. ^ Brüssow H, Canchaya C, Hardt WD (September 2004). "Phages and the evolution of bacterial pathogens: from genomic rearrangements to lysogenic conversion". Microbiol. Mol. Biol. Rev. 68 (3): 560–602. doi:10.1128/MMBR.68.3.560-602.2004. PMC 515249. PMID 15353570. 
  21. ^ Krieg, N. R.; Holt, J. G., eds. (1984). Bergey's Manual of Systematic Bacteriology 1 (First ed.). Baltimore: The Williams & Wilkins Co. pp. 408–420. ISBN 0-683-04108-8. 
  22. ^ a b c Lukjancenko O, Wassenaar TM, Ussery DW (November 2010). "Comparison of 61 sequenced Escherichia coli genomes". Microb. Ecol. 60 (4): 708–20. doi:10.1007/s00248-010-9717-3. PMC 2974192. PMID 20623278. 
  23. ^ Lan R, Reeves PR (September 2002). "Escherichia coli in disguise: molecular origins of Shigella". Microbes Infect. 4 (11): 1125–32. doi:10.1016/S1286-4579(02)01637-4. PMID 12361912. 
  24. ^ Orskov I, Orskov F, Jann B, Jann K (September 1977). "Serology, chemistry, and genetics of O and K antigens of Escherichia coli". Bacteriol Rev 41 (3): 667–710. PMC 414020. PMID 334154. 
  25. ^ Stenutz, R.; Weintraub, A.; Widmalm, G. (2006). "The structures of Escherichia coli O-polysaccharide antigens". FEMS Microbiol Rev 30 (3): 382–403. doi:10.1111/j.1574-6976.2006.00016.x. PMID 16594963 
  26. ^ Lawrence JG, Ochman H (August 1998). "Molecular archaeology of the Escherichia coli genome". Proc. Natl. Acad. Sci. U.S.A. 95 (16): 9413–7. Bibcode:1998PNAS...95.9413L. doi:10.1073/pnas.95.16.9413. PMC 21352. PMID 9689094. 
  27. ^ a b Nataro JP, Kaper JB (January 1998). "Diarrheagenic Escherichia coli". Clin. Microbiol. Rev. 11 (1): 142–201. PMC 121379. PMID 9457432. 
  28. ^ a b Brenner, Don J.; Krieg, Noel R.; Staley, James T. (July 26, 2005) [1984 (Williams & Wilkins)]. George M. Garrity, ed. The Gammaproteobacteria. Bergey's Manual of Systematic Bacteriology 2B (2nd ed.). New York: Springer. p. 1108. ISBN 978-0-387-24144-9. British Library no. GBA561951. 
  29. ^ Discussion of nomenclature of Enterobacteriaceae entry in LPSN [Euzéby, J.P. (1997). "List of Bacterial Names with Standing in Nomenclature: a folder available on the Internet". Int J Syst Bacteriol 47 (2): 590–2. doi:10.1099/00207713-47-2-590. ISSN 0020-7713. PMID 9103655. ]
  30. ^ International Bulletin of Bacteriological Nomenclature and Taxonomy 8:73–74 (1958)
  31. ^ http://www.atcc.org/ATCCAdvancedCatalogSearch/ProductDetails/tabid/452/Default.aspx?ATCCNum=11775&Template=bacteria
  32. ^ "Escherichia". bacterio.cict.fr. 
  33. ^ "Escherichia coli (Migula 1895) Castellani and Chalmers 1919". JCM Catalogue. 
  34. ^ Brzuszkiewicz E, Thürmer A, Schuldes J, Leimbach A, Liesegang H, Meyer FD, Boelter J, Petersen H, Gottschalk G, Daniel R (December 2011). "Genome sequence analyses of two isolates from the recent Escherichia coli outbreak in Germany reveal the emergence of a new pathotype: Entero-Aggregative-Haemorrhagic Escherichia coli (EAHEC)". Arch. Microbiol. 193 (12): 883–91. doi:10.1007/s00203-011-0725-6. PMC 3219860. PMID 21713444. 
  35. ^ a b Blattner FR, Plunkett G, Bloch CA, Perna NT, Burland V, Riley M, Collado-Vides J, Glasner JD, Rode CK, Mayhew GF, Gregor J, Davis NW, Kirkpatrick HA, Goeden MA, Rose DJ, Mau B, Shao Y (September 1997). "The complete genome sequence of Escherichia coli K-12". Science 277 (5331): 1453–62. doi:10.1126/science.277.5331.1453. PMID 9278503. 
  36. ^ Zhaxybayeva O, Doolittle WF (April 2011). "Lateral gene transfer". Curr. Biol. 21 (7): R242–6. doi:10.1016/j.cub.2011.01.045. PMID 21481756. 
  37. ^ Han, M. J.; Lee, S. Y. (2006). "The Escherichia coli proteome: Past, present, and future prospects". Microbiology and Molecular Biology Reviews 70 (2): 362–439. doi:10.1128/MMBR.00036-05. PMC 1489533. PMID 16760308.  edit
  38. ^ Arifuzzaman M, Maeda M, Itoh A, Nishikata K, Takita C, Saito R, Ara T, Nakahigashi K, Huang HC, Hirai A, Tsuzuki K, Nakamura S, Altaf-Ul-Amin M, Oshima T, Baba T, Yamamoto N, Kawamura T, Ioka-Nakamichi T, Kitagawa M, Tomita M, Kanaya S, Wada C, Mori H (May 2006). "Large-scale identification of protein-protein interaction of Escherichia coli K-12". Genome Res. 16 (5): 686–91. doi:10.1101/gr.4527806. PMC 1457052. PMID 16606699. 
  39. ^ Hu P, Janga SC, Babu M, Díaz-Mejía JJ, Butland G, Yang W, Pogoutse O, Guo X, Phanse S, Wong P, Chandran S, Christopoulos C, Nazarians-Armavil A, Nasseri NK, Musso G, Ali M, Nazemof N, Eroukova V, Golshani A, Paccanaro A, Greenblatt JF, Moreno-Hagelsieb G, Emili A (April 2009). "Global functional atlas of Escherichia coli encompassing previously uncharacterized proteins". In Levchenko, Andre. PLoS Biol. 7 (4): e96. doi:10.1371/journal.pbio.1000096. PMC 2672614. PMID 19402753. 
  40. ^ Rajagopala, S. V.; Sikorski, P; Kumar, A; Mosca, R; Vlasblom, J; Arnold, R; Franca-Koh, J; Pakala, S. B.; Phanse, S; Ceol, A; Häuser, R; Siszler, G; Wuchty, S; Emili, A; Babu, M; Aloy, P; Pieper, R; Uetz, P (2014). "The binary protein-protein interaction landscape of Escherichia coli". Nature Biotechnology 32 (3): 285–90. doi:10.1038/nbt.2831. PMID 24561554.  edit
  41. ^ a b Todar, K. "Pathogenic E. coli". Online Textbook of Bacteriology. University of Wisconsin–Madison Department of Bacteriology. Retrieved 2007-11-30. 
  42. ^ Evans Jr., Doyle J.; Dolores G. Evans. "Escherichia Coli". Medical Microbiology, 4th edition. The University of Texas Medical Branch at Galveston. Archived from the original on 2007-11-02. Retrieved 2007-12-02. 
  43. ^ Lodinová-Zádníková R, Cukrowska B, Tlaskalova-Hogenova H. Oral administration of probiotic Escherichia coli after birth reduces frequency of allergies and repeated infections later in life (after 10 and 20 years). Int Arch Allergy Immunol. 2003 Jul;131(3):209-11. PubMed PMID 12876412.
  44. ^ Grozdanov L, Raasch C, Schulze J, Sonnenborn U, Gottschalk G, Hacker J, Dobrindt U (August 2004). "Analysis of the genome structure of the nonpathogenic probiotic Escherichia coli strain Nissle 1917". J. Bacteriol. 186 (16): 5432–41. doi:10.1128/JB.186.16.5432-5441.2004. PMC 490877. PMID 15292145. 
  45. ^ Kamada N, Inoue N, Hisamatsu T, Okamoto S, Matsuoka K, Sato T, Chinen H, Hong KS, Yamada T, Suzuki Y, Suzuki T, Watanabe N, Tsuchimoto K, Hibi T (May 2005). "Nonpathogenic Escherichia coli strain Nissle1917 prevents murine acute and chronic colitis". Inflamm. Bowel Dis. 11 (5): 455–63. doi:10.1097/01.MIB.0000158158.55955.de. PMID 15867585. 
  46. ^ http://www.mayoclinic.org/diseases-conditions/e-coli/basics/definition/con-20032105
  47. ^ a b "Uropathogenic Escherichia coli: The Pre-Eminent Urinary Tract Infection Pathogen". Nova publishers. Retrieved 27 November 2013. 
  48. ^ Enterohemorrhagic Escherichia Coli (EHEC) outbreak in Germany
  49. ^ "Samen von Bockshornklee mit hoher Wahrscheinlichkeit für EHEC O104:H4 Ausbruch verantwortlich in English: Fenugreek seeds with high probability for EHEC O104: H4 responsible outbreak" (PDF) (in German). Bundesinstitut für Risikobewertung (BfR) in English: Federal Institute for Risk Assessment. 30 June 2011. Retrieved 17 July 2011. 
  50. ^ Lee SY (1996). "High cell-density culture of Escherichia coli". Trends Biotechnol. 14 (3): 98–105. doi:10.1016/0167-7799(96)80930-9. PMID 8867291. 
  51. ^ Russo E (January 2003). "The birth of biotechnology". Nature 421 (6921): 456–457. Bibcode:2003Natur.421..456R. doi:10.1038/nj6921-456a. PMID 12540923. 
  52. ^ a b Cornelis P (2000). "Expressing genes in different Escherichia coli compartments". Curr. Opin. Biotechnol. 11 (5): 450–454. doi:10.1016/S0958-1669(00)00131-2. PMID 11024362. 
  53. ^ Tof, Ilanit (1994). "Recombinant DNA Technology in the Synthesis of Human Insulin". Little Tree Pty. Ltd. Retrieved 2007-11-30. 
  54. ^ Bessette PH, Aslund F, Beckwith J, Georgiou G (November 1999). "Efficient folding of proteins with multiple disulfide bonds in the Escherichia coli cytoplasm". Proc. Natl. Acad. Sci. U.S.A. 96 (24): 13703–8. Bibcode:1999PNAS...9613703B. doi:10.1073/pnas.96.24.13703. PMC 24128. PMID 10570136. 
  55. ^ Ihssen J, Kowarik M, Dilettoso S, Tanner C, Wacker M, Thöny-Meyer L. (2010). "Production of glycoprotein vaccines in Escherichia coli". Microbial Cell Factories 9 (61): 494–7. doi:10.1186/1475-2859-9-61. PMC 2927510. PMID 20701771. 
  56. ^ Wacker M, Linton D, Hitchen PG, Nita-Lazar M, Haslam SM, North SJ, Panico M, Morris HR, Dell A, Wren BW, Aebi M (2002). "N-linked glycosylation in Campylobacter jejuni and its functional transfer into E. coli". Science 298 (5599): 1790–1793. doi:10.1126/science.298.5599.1790. PMID 12459590. 
  57. ^ Huang CJ, Lin H, Yang X. (2012). "Industrial production of recombinant therapeutics in Escherichia coli and its recent advancements". J Ind Microbiol Biotechnol 39 (3): 383–99. doi:10.1007/s10295-011-1082-9. PMID 22252444. 
  58. ^ Summers, Rebecca (24 April 2013) Bacteria churn out first ever petrol-like biofuel New Scientist, Retrieved 27 April 2013
  59. ^ Nic Halverson (August 15, 2013). "Bacteria-Powered Light Bulb Is Electricity-Free". 
  60. ^ Fux CA, Shirtliff M, Stoodley P, Costerton JW (2005). "Can laboratory reference strains mirror "real-world" pathogenesis?". Trends Microbiol. 13 (2): 58–63. doi:10.1016/j.tim.2004.11.001. PMID 15680764. 
  61. ^ Vidal O, Longin R, Prigent-Combaret C, Dorel C, Hooreman M, Lejeune P (1998). "Isolation of an Escherichia coli K-12 mutant strain able to form biofilms on inert surfaces: involvement of a new ompR allele that increases curli expression". J. Bacteriol. 180 (9): 2442–9. PMC 107187. PMID 9573197. 
  62. ^ Lederberg, Joshua; E.L. Tatum (October 19, 1946). "Gene recombination in E. coli" (PDF). Nature 158 (4016): 558. Bibcode:1946Natur.158..558L. doi:10.1038/158558a0.  Source: National Library of Medicine – The Joshua Lederberg Papers
  63. ^ Biological Activity of Crystal. p. 169. 
  64. ^ "The Phage Course – Origins". Cold Spring Harbor Laboratory. 2006. Retrieved 2007-12-03. [dead link]
  65. ^ Benzer S (March 1961). "ON THE TOPOGRAPHY OF THE GENETIC FINE STRUCTURE". Proc. Natl. Acad. Sci. U.S.A. 47 (3): 403–15. Bibcode:1961PNAS...47..403B. doi:10.1073/pnas.47.3.403. PMC 221592. PMID 16590840. 
  66. ^ "Facts about E.Coli". Encyclopedia of Life. Retrieved 27 November 2013. 
  67. ^ Bacteria make major evolutionary shift in the lab New Scientist
  68. ^ Keymer JE, Galajda P, Muldoon C, Park S, Austin RH (November 2006). "Bacterial metapopulations in nanofabricated landscapes". Proc. Natl. Acad. Sci. U.S.A. 103 (46): 17290–5. Bibcode:2006PNAS..10317290K. doi:10.1073/pnas.0607971103. PMC 1635019. PMID 17090676. 
  69. ^ Baumgardner, J; Acker, K; Adefuye, O; Crowley, ST; Deloache, W; Dickson, JO; Heard, L; Martens, AT; Morton, N; Ritter, M; Shoecraft, A; Treece, J; Unzicker, M; Valencia, A; Waters, M; Campbell, AM; Heyer, LJ; Poet, JL; Eckdahl, TT (July 24, 2009). "Solving a Hamiltonian Path Problem with a bacterial computer". Journal of Biological Engineering (J Biol Eng. 2009; 3: 11.) 3: 11. doi:10.1186/1754-1611-3-11. PMC 2723075. PMID 19630940. 
  70. ^ Battistuzzi FU, Feijao A, Hedges SB (November 2004). "A genomic timescale of prokaryote evolution: insights into the origin of methanogenesis, phototrophy, and the colonization of land". BMC Evol. Biol. 4: 44. doi:10.1186/1471-2148-4-44. PMC 533871. PMID 15535883. 
  71. ^ Lecointre G, Rachdi L, Darlu P, Denamur E (December 1998). "Escherichia coli molecular phylogeny using the incongruence length difference test". Mol. Biol. Evol. 15 (12): 1685–95. doi:10.1093/oxfordjournals.molbev.a025895. PMID 9866203. 
  72. ^ Haeckel, Ernst (1867). Generelle Morphologie der Organismen. Reimer, Berlin. ISBN 1-144-00186-2. 
  73. ^ Escherich T (1885). "Die Darmbakterien des Neugeborenen und Säuglinge". Fortschr. Med. 3: 515–522. 
  74. ^ Breed RS, Conn HJ (May 1936). "The Status of the Generic Term Bacterium Ehrenberg 1828". J. Bacteriol. 31 (5): 517–8. PMC 543738. PMID 16559906. 
  75. ^ MIGULA (W.): Bacteriaceae (Stabchenbacterien). In: A. ENGLER and K. PRANTL (eds): Die Naturlichen Pfanzenfamilien, W. Engelmann, Leipzig, Teil I, Abteilung Ia, 1895, pp. 20–30.
  76. ^ CASTELLANI (A.) and CHALMERS (A.J.): Manual of Tropical Medicine, 3rd ed., Williams Wood and Co., New York, 1919.
Creative Commons Attribution Share Alike 3.0 (CC BY-SA 3.0)

Source: Wikipedia

Unreviewed

Article rating from 0 people

Default rating: 2.5 of 5

Escherichia coli (molecular biology)

For general article about E. coli as a species, see Escherichia coli.

Escherichia coli (/ˌɛʃɨˈrɪkiə ˈkl/; commonly abbreviated E. coli) is a gammaproteobacterium commonly found in the lower intestine of warm-blooded organisms (endotherms). The descendants of two isolates, K-12 and B strain, are used routinely in molecular biology as both a tool and a model organism.

Diversity of Escherichia coli[edit]

Escherichia coli is one of the most diverse bacterial species with several pathogenic strains with different symptoms and with only 20% of the genome common to all strains.[1] Furthermore, from the evolutionary point of view, the members of genus Shigella (dysenteriae, flexneri, boydii, sonnei) are actually E. coli strains "in disguise" (i.e. E. coli is paraphyletic to the genus).[2]

History[edit]

In 1885, Theodor Escherich, a German pediatrician, first discovered this species in the feces of healthly individuals and called it Bacterium coli commune due to the fact it is found in the colon and early classifications of Prokaryotes placed these in a handful of genera based on their shape and motility (at that time Ernst Haeckel's classification of Bacteria in the kingdom Monera was in place[3]).[4]

Following a revision of Bacteria it was reclassified as Bacillus coli by Migula in 1895[5] and later reclassified as Escherichia coli [6]

Due to its ease of culture and fast doubling it was used in the early microbiology experiments, however bacteria were considered primitive and pre-cellular and received little attention before 1944, when Avery, Macleod and McCarty demonstrated that DNA was the genetic material using Salmonella typhimurium, following which Escherichia coli was used for linkage mapping studies [7]

Strains[edit]

Four of the many E.coli strains (K-12, B, C, and W) are thought of as model organism strains. These are classified in Risk Group 1 in biosafety guidelines.

Escherich's isolate[edit]

The first isolate of Escherich was deposited in NCTC in 1920 by the Lister Institute in London (NCTC 86[1].[8]

K-12[edit]

A strain was isolated from a stool sample of a patient convalescent from diphtheria and was labelled K-12 (not an antigen) in 1922 at Stanford University.[9] This isolate was used in 1940s by Charles E. Clifton to study nitrogen metabolism who deposited it in ATCC (strain ATCC 10798) and lent it to Edward Tatum for his tryptophan biosynthesis experiments,[10] despite its idiosyncrasies due to the F+ λ+ phenotype.[7] In the course of the passages it lost its O antigen[7] and in 1953 was cured first of its lambda phage (strain W1485 by UV by Joshua Lederberg and colleagues) and then in 1985 of the F plasmid by acridine orange curing .[citation needed] Strains derived from MG1655 include DH1, parent of DH5α and in turn of DH10β (rebranded as TOP10 by Invitrogen[11]).[12] An alternative lineage from W1485 is that of W2637 (which contains an inversion rrnD-rrnE), which in turn resulted in W3110.[8] Due to the lack of specific record-keeping, the "pedigree" of strains was not available and had to be inferred by consulting lab-book and records in order to set up the E. coli Genetic Stock Centre at Yale.[9] The different strains have been derived through treating E. coli K-12 with agents such as nitrogen mustard, ultra-violet radiation, X-ray etc. An extensive list of Escherichia coli K-12 strain derivatives and their individual construction, genotypes, phenotypes, plasmids and phage information can be viewed at Ecoliwiki.

B strain[edit]

A second common laboratory strain is the B strain, whose history is less straightforward and the first naming of the strain as E. coli B was by Delbrück and Luria in 1942 in their study of bacteriophages T1 and T7 [13] The original E. coli B strain, known then as Bacillus coli, originated from Félix d'Herelle from the Institut Pasteur in Paris around 1918 who studied bacteriophages,[14] who claimed that it originated from Collection of the Institut Pasteur,[15] but no strains of that period exist.[8] The strain of d'Herelle was passed to Jules Bordet, Director of the Institut Pasteur du Brabant in Bruxelles[16] and his student André Gratia [17] The former passed the strain to Ann Kuttner ("the Bact. coli obtained from Dr. Bordet")[18] and in turn to Eugène Wollman (B. coli Bordet),[19] whose son deposited it in 1963 (CIP 63.70) as "strain BAM" (B American), while André Gratia passed the strain to Martha Wollstein, a researcher at Rockefeller, who refers to the strain as "Brussels strain of Bacillus coli" in 1921,[20] who in turn passed it to Jacques Bronfenbrenner (B. coli P.C.), who passed it to Delbrück and Luria.[8][13] This strain gave rise to several other strains, such as REL606 and BL21.[8]

C strain[edit]

E. coli C is morphologically distinct from other E. coli strains; it is more spherical in shape and has a distinct distribution of its nucleoid.[21]

W strain[edit]

The W strain was isolated from the soil near Rutgers University's by Selman Waksman[22]

Role in biotechnology[edit]

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.[23] The work of Stanley Norman Cohen and Herbert Boyer in E. coli, using plasmids and restriction enzymes to create recombinant DNA, became a foundation of biotechnology.[24]

Considered a very versatile host for the production of heterologous proteins,[25] researchers can introduce genes into the microbes using plasmids, allowing for the mass production of proteins in 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.[26] Modified E. coli have been used in vaccine development, bioremediation, and production of immobilised enzymes.[25]

E. coli have been used successfully to produce proteins previously thought difficult or impossible in E. coli, such as those containing multiple disulfide bonds or those requiring post-translational modification for stability or function. The cellular environment of E. coli is normally too reducing for disulphide bonds to form, proteins with disulphide bonds therefore may be secreted to its periplasmic space, however, mutants in which the reduction of both thioredoxins and glutathione is impaired also allow disulphide bonded proteins to be produced in the cytoplasm of E. coli.[27] It has also been use to produce proteins with various post-translational modifications, including glycoproteins by using the N-linked glycosylation system of Campylobacter jejuni engineered into E. coli.[28][29] Efforts are currently under way to expand this technology to produce complex glycosylations.[30][31]

Studies are also being performed into programming E. coli to potentially solve complicated mathematics problems such as the Hamiltonian path problem.[32]


Model organism[edit]

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.[33][34] 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,[35] and it remains a primary model to study conjugation.[36] E. coli was an integral part of the first experiments to understand phage genetics,[37] and early researchers, such as Seymour Benzer, used E. coli and phage T4 to understand the topography of gene structure.[38] Prior to Benzer's research, it was not known whether the gene was a linear structure, or if it had a branching pattern.

E. coli was one of the first organisms to have its genome sequenced; the complete genome of E. coli K-12 was published by Science in 1997.[39] Available genome sequences include Escherichia coli str. K-12 substr. MG1655 and Escherichia coli O157:H7 str. Sakai.

Lenski's long term evolution experiment[edit]

The long-term evolution experiments using E. coli, begun by Richard Lenski in 1988, have allowed direct observation of major evolutionary shifts in the laboratory.[40] In this experiment, one population of E. coli unexpectedly evolved the ability to aerobically metabolize citrate. This capacity is extremely rare in E. coli. As the inability to grow aerobically is normally used as a diagnostic criterion with which to differentiate E. coli from other, closely related bacteria such as Salmonella, this innovation may mark a speciation event observed in the lab.

References[edit]

  1. ^ Lukjancenko, O.; Wassenaar, T.M.; Ussery, D.W. (2010). "Comparison of 61 sequenced Escherichia coli genomes". Microb Ecol. 60 (4): 708–720. doi:10.1007/s00248-010-9717-3. PMC 2974192. PMID 20623278. 
  2. ^ Lan, R.; Reeves, P.R. (2002). "Escherichia coli in disguise: molecular origins of Shigella". Microbes Infect. 4 (11): 1125–1132. doi:10.1016/S1286-4579(02)01637-4. PMID 12361912. 
  3. ^ Haeckel, Ernst (1867). Generelle Morphologie der Organismen. Reimer, Berlin. ISBN 1-144-00186-2. 
  4. ^ Escherich T (1885). "Die Darmbakterien des Neugeborenen und Säuglinge". Fortschr. Med. 3: 515–522. 
  5. ^ MIGULA (W.): Bacteriaceae (Stabchenbacterien). In: A. ENGLER and K. PRANTL (eds): Die Naturlichen Pfanzenfamilien, W. Engelmann, Leipzig, Teil I, Abteilung Ia, 1895, pp. 20–30.
  6. ^ CASTELLANI (A.) and CHALMERS (A.J.): Manual of Tropical Medicine, 3rd ed., Williams Wood and Co., New York, 1919.
  7. ^ a b c Lederber, J. 2004 E. coli K-12. Microbiology today 31:116
  8. ^ a b c d e Daegelen, P.; Studier, F. W.; Lenski, R. E.; Cure, S.; Kim, J. F. (2009). "Tracing Ancestors and Relatives of Escherichia coli B, and the Derivation of B Strains REL606 and BL21(DE3)". Journal of Molecular Biology 394 (4): 634–643. doi:10.1016/j.jmb.2009.09.022. PMID 19765591.  edit
  9. ^ a b Bachmann, B. J. (1972). "Pedigrees of some mutant strains of Escherichia coli K-12". Bacteriological reviews 36 (4): 525–557. PMC 408331. PMID 4568763.  edit
  10. ^ Tatum E. L., Lederberg J. (1947). "Gene recombination in the bacterium Escherichia coli". J. Bacteriol 53: 673–684. 
  11. ^ E. coli genotypes – OpenWetWare
  12. ^ Meselson, M; Yuan, R (1968). "DNA restriction enzyme from E. Coli". Nature 217 (5134): 1110–4. Bibcode:1968Natur.217.1110M. doi:10.1038/2171110a0. PMID 4868368.  edit
  13. ^ a b Delbrück M., Luria S. E. (1942). "Interference between bacterial viruses: I. Interference between two bacterial viruses acting upon the same host, and the mechanism of virus growth". Arch. Biochem 1: 111–141. 
  14. ^ D'Herelle F (1918). "Sur le rôle du microbe filtrant bactériophage dans la dysenterie bacillaire". Compt. Rend. Acad. Sci. 167: 970–972. 
  15. ^ d'Herelle, F. (1926). In Le bactériophage et son comportement. Monographies de l'Institut Pasteur, Masson et Cie, Libraires de l'Académie de Médecine, 120,Boulevard Saint Germain, Paris-VIe, France.
  16. ^ Bordet J., Ciuca M. (1920). "Le bactériophage de d'Herelle, sa production et son interprétation". Compt. Rend. Soc. Biol. 83: 1296–1298. 
  17. ^ Gratia A., Jaumain D. (1921). "Dualité du principe lytique du colibacille et du staphylococque". Compt. Rend. Soc. Biol. 84: 882–884. 
  18. ^ Kuttner A. G. (1923). "Bacteriophage phenomena". J. Bacteriol 8 (1): 49–101. PMC 379003. PMID 16558985. 
  19. ^ Wollman E (1925). "Recherches sur la bactériophagie (phénomène de Twort-d'Hérelle)". Ann. Inst. Pasteur 39: 789–832. 
  20. ^ Wollstein M (1921). "Studies on the phenomenon of d'Herelle with Bacillus dysenteriae". J. Exp. Med. 35: 467–476. doi:10.1084/jem.34.5.467. PMC 2128695. PMID 19868572. 
  21. ^ Lieb, M.; Weigle, J. J.; Kellenberger, E. (1955). "A study of hybrids between two strains of Escherichia coli". Journal of bacteriology 69 (4): 468–471. PMC 357561. PMID 14367303.  edit
  22. ^ Colin T Archer, Jihyun F Kim, Haeyoung Jeong, Jin H Park, Claudia E Vickers, Sang Y Lee and Lars K Nielsen (2011). "The genome sequence of E. coli W (ATCC 9637): comparative genome analysis and an improved genome-scale reconstruction of E. coli". BMC Genomics 12. doi:10.1186/1471-2164-12-9. PMID 21208457. 
  23. ^ Lee SY (1996). "High cell-density culture of Escherichia coli". Trends Biotechnol. 14 (3): 98–105. doi:10.1016/0167-7799(96)80930-9. PMID 8867291. 
  24. ^ Russo E (January 2003). "The birth of biotechnology". Nature 421 (6921): 456–7. Bibcode:2003Natur.421..456R. doi:10.1038/nj6921-456a. PMID 12540923. 
  25. ^ a b Cornelis P (2000). "Expressing genes in different Escherichia coli compartments". Current Opinion in Biotechnology 11 (5): 450–4. doi:10.1016/S0958-1669(00)00131-2. PMID 11024362. 
  26. ^ Tof, Ilanit (1994). "Recombinant DNA Technology in the Synthesis of Human Insulin". Little Tree Pty. Ltd. Retrieved 2007-11-30. 
  27. ^ Paul H. Bessette, Fredrik Åslund, Jon Beckwith, and George Georgiou (1999). "Efficient folding of proteins with multiple disulfide bonds in the Escherichia coli cytoplasm". Proc. Natl. Acad. Sci. U.S.A. 96 (24): 13703–8. doi:10.1073/pnas.96.24.13703. PMC 24128. PMID 10570136. 
  28. ^ Ihssen J, Kowarik M, Dilettoso S, Tanner C, Wacker M, Thöny-Meyer L. (2010). "Production of glycoprotein vaccines in Escherichia coli". Microbial Cell Factories 9 (61): 494–7. doi:10.1186/1475-2859-9-61. PMC 2927510. PMID 20701771. 
  29. ^ Wacker M, Linton D, Hitchen PG, Nita-Lazar M, Haslam SM, North SJ, Panico M, Morris HR, Dell A, Wren BW, Aebi M (2002). "N-linked glycosylation in Campylobacter jejuni and its functional transfer into E. coli". Science 298 (5599): 1790–1793. doi:10.1126/science.298.5599.1790. PMID 12459590. 
  30. ^ Valderrama-Rincon JD, Fisher AC, Merritt JH, Fan YY, Reading CA, Chhiba K, Heiss C, Azadi P, Aebi M, Delisa MP. (2012). "An engineered eukaryotic protein glycosylation pathway in Escherichia coli.". Nat Chem Biol. 8 (5): 434–6. doi:10.1038/nchembio.921. PMID 22446837. 
  31. ^ Huang CJ, Lin H, Yang X. (2012). "Industrial production of recombinant therapeutics in Escherichia coli and its recent advancements". J Ind Microbiol Biotechnol 39 (3): 383–99. doi:10.1007/s10295-011-1082-9. PMID 22252444. 
  32. ^ "E. coli can solve math problems". The Deccan Chronicle. July 26, 2009. Retrieved July 26, 2009. 
  33. ^ Fux CA, Shirtliff M, Stoodley P, Costerton JW (2005). "Can laboratory reference strains mirror "real-world" pathogenesis?". Trends Microbiol. 13 (2): 58–63. doi:10.1016/j.tim.2004.11.001. PMID 15680764. 
  34. ^ Vidal O, Longin R, Prigent-Combaret C, Dorel C, Hooreman M, Lejeune P (1998). "Isolation of an Escherichia coli K-12 mutant strain able to form biofilms on inert surfaces: involvement of a new ompR allele that increases curli expression". J. Bacteriol. 180 (9): 2442–9. PMC 107187. PMID 9573197. 
  35. ^ Lederberg, Joshua; E.L. Tatum (October 19, 1946). "Gene recombination in E. coli" (PDF). Nature 158 (4016): 558. Bibcode:1946Natur.158..558L. doi:10.1038/158558a0.  Source: National Library of Medicine – The Joshua Lederberg Papers
  36. ^ F Xavier Gomis-Rüth, Miquel Coll (December 2006). "Cut and move: protein machinery for DNA processing in bacterial conjugation". Current Opinion in Structural Biology 16 (6): 744–752. doi:10.1016/j.sbi.2006.10.004. PMID 17079132. 
  37. ^ "The Phage Course – Origins". Cold Spring Harbor Laboratory. 2006. Retrieved 2007-12-03. [dead link]
  38. ^ Benzer, Seymour (March 1961). "On the topography of the genetic fine structure". PNAS 47 (3): 403–15. Bibcode:1961PNAS...47..403B. doi:10.1073/pnas.47.3.403. PMC 221592. PMID 16590840. 
  39. ^ Frederick R. Blattner, Guy Plunkett III, Craig Bloch, Nicole Perna, Valerie Burland, Monica Riley, Julio Collado-Vides, Jeremy Glasner, Christopher Rode, George Mayhew, Jason Gregor, Nelson Davis, Heather Kirkpatrick, Michael Goeden, Debra Rose, Bob Mau, Ying Shao (September 5, 1997). "The complete genome sequence of Escherichia coli K-12". Science 277 (5331): 1453–1462. doi:10.1126/science.277.5331.1453. PMID 9278503. 
  40. ^ Bacteria make major evolutionary shift in the lab New Scientist
Creative Commons Attribution Share Alike 3.0 (CC BY-SA 3.0)

Source: Wikipedia

Unreviewed

Article rating from 0 people

Default rating: 2.5 of 5

Pathogenic Escherichia coli

Escherichia coli (/ˌɛʃəˈrɪkiə ˈklɪ/ Anglicized to /ˌɛʃəˈrɪkiə ˈkl/; commonly abbreviated E. coli) is a gram-negative, rod-shaped bacterium that is commonly found in the lower intestine of warm-blooded organisms (endotherms). Most E. coli strains are harmless, but some serotypes are pathogenic and can cause serious food poisoning in humans, and are occasionally responsible for 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,[3] and by preventing the establishment of pathogenic bacteria within the intestine.[4][5]

Introduction[edit]

E. coli and related bacteria constitute about 0.1% of gut flora,[6] and fecal–oral transmission is the major route through which pathogenic strains of the bacterium cause disease. Cells are able to survive outside the body for a limited amount of time, which makes them ideal indicator organisms to test environmental samples for fecal contamination.[7][8] The bacterium can also be grown easily and inexpensively in a laboratory setting, and has been intensively investigated for over 60 years. E. coli is the most widely studied prokaryotic model organism, and an important species in the fields of biotechnology and microbiology, where it has served as the host organism for the majority of work with recombinant DNA.

German paediatrician and bacteriologist Theodor Escherich discovered E. coli in 1885,[7] and it is now classified as part of the Enterobacteriaceae family of gamma-proteobacteria.[9]

Serotypes[edit]

Structure of a lipopolysaccharide

Pathogenic E.coli strains can be categorised based on elements that can elicit an immune response in animals, namely:

  1. O antigen: part of lipopolysaccharide layer
  2. K antigen: capsule
  3. H antigen: flagellin

For example E.coli strain EDL933 is of the O157:H7 group.

O antigen[edit]

Main article: O antigen

The outer membrane of an E. coli cell contains millions of lipopolysaccharide (LPS) molecules, which consists of:

  1. O antigen, a polymer of immunogenic repeating oligosaccharides (1–40 units)
  2. Core region of phosphorylated nonrepeating oligosaccharides
  3. Lipid A (endotoxin)

The O antigen is used for serotyping E.coli and these O group designations go from O1 to O181, with the exception of some groups which have been historically removed, namely O31, O47, O67, O72, O93 (now K84), O94, and O122; groups 174 to 181 are provisional (O174=OX3 and O175=OX7) or are under investigation (176 to 181 are STEC/VTEC).[10] Additionally subtypes exist for many O groups (e.g. O128ab and O128ac).[10] It should be noted though that antibodies towards several O antigens cross-react with other O antigens and partially to K antigens not only from E. coli, but also from other Escherichia species and Enterobacteriaceae species.[10]

The O antigen is encoded by the rfb gene cluster. rol (cld) gene encodes the regulator of lipopolysaccharide O-chain length.

K antigen[edit]

The acidic capsular polysaccharide (CPS) is a thick, mucous-like, layer of polysaccharide that surrounds some pathogen E. coli.

There are two separate groups of K-antigen groups, named group I and group II (while a small in-between subset (K3, K10, and K54/K96) has been classified as group III).[10] The former (I) consist of 100 kDa (large) capsular polysaccharides, while the latter (II), associated with extraintestinal diseases, are under 50 kDa in size.[10]

Group I K antigens are only found with certain O-antigens (O8, O9, O20, and O101 groups), they are further subdivided on the basis of absence (IA, similar to that of Klebsiella species in structure) or presence (IB) of amino sugars and some group I K-antigens are attached to the lipid A-core of the lipopolysaccharide (KLPS), in a similar way to O antigens (and being structurally identical to O antigens in some instances are only considered as K antigens when co-expressed with another authentic O antigen).[10]

Group II K antigens closely resemble those in gram-positive bacteria and greatly differ in composition and are further subdivided according to their acidic components, generally 20–50% of the CPS chains are bound to phospholipids.[10]

In total there are 60 different K antigens that have been recognized (K1, K2a/ac, K3, K4, K5, K6, K7 (=K56), K8, K9 (=O104), K10, K11, K12 (K82), K13(=K20 and =K23), K14, K15, K16, K18a, K18ab (=K22), K19,K24, K26, K27, K28, K29, K30, K31, K34, K37, K39, K40, K41,K42, K43, K44, K45, K46, K47, K49 (O46), K50, K51, K52, K53, K54 (=K96), K55, K74, K84, K85ab/ac (=O141), K87 (=O32), K92, K93, K95, K97, K98, K100, K101, K102, K103, KX104, KX105,and KX106).

H antigen[edit]

See also: flagella

The flagella allows E. coli to move. H antigens groups go from H1 to H56 with some exceptions (H13 and H22 were not E. coli antigens but from Citrobacter freundii, also a coliform, and H50 being the same as H10). These are encoded by the fliC gene.

Role in disease[edit]

In humans and in domestic animals, virulent strains of E. coli can cause various diseases.

In humans : gastroenteritis, urinary tract infections, and neonatal meningitis. In rarer cases, virulent strains are also responsible for haemolytic-uremic syndrome, peritonitis, mastitis, septicaemia and gram-negative pneumonia.[11]

Gastrointestinal infection[edit]

Low-temperature electron micrograph of a cluster of E. coli bacteria, magnified 10,000 times. Each individual bacterium is a rounded cylinder.

Certain strains of E. coli, such as O157:H7, O104:H4, O121, O26, O103, O111, O145, and O104:H21, produce potentially lethal toxins. Food poisoning caused by E. coli can result from eating unwashed vegetables or poorly butchered and undercooked meat. O157:H7 is also notorious for causing serious and even life-threatening complications such as hemolytic-uremic syndrome. This particular strain is linked to the 2006 United States E. coli outbreak due to fresh spinach. The O104:H4 strain is equally virulent. Antibiotic and supportive treatment protocols for it are not as well-developed (it has the ability to be very enterohemorrhagic like O157:H7, causing bloody diarrhea, but also is more enteroaggregative, meaning it adheres well and clumps to intestinal membranes). It is the strain behind the deadly June 2011 E. coli outbreak in Europe. Severity of the illness varies considerably; it can be fatal, particularly to young children, the elderly or the immunocompromised, but is more often mild. Earlier, poor hygienic methods of preparing meat in Scotland killed seven people in 1996 due to E. coli poisoning, and left hundreds more infected. E. coli can harbour both heat-stable and heat-labile enterotoxins. The latter, termed LT, contain one A subunit and five B subunits arranged into one holotoxin, and are 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.[12]

If E. coli bacteria escape the intestinal tract through a perforation (for example from an ulcer, a ruptured appendix, or due to a surgical error) and enter the abdomen, they usually cause peritonitis that can be fatal without prompt treatment. However, E. coli are extremely sensitive to such antibiotics as streptomycin or gentamicin. Recent research suggests treatment of enteropathogenic E. coli with antibiotics may not improve the outcome of the disease,[citation needed] as it may significantly increase the chance of developing haemolytic-uremic syndrome.[13]

Intestinal mucosa-associated E. coli are observed in increased numbers in the inflammatory bowel diseases, Crohn's disease and ulcerative colitis.[14] Invasive strains of E. coli exist in high numbers in the inflamed tissue, and the number of bacteria in the inflamed regions correlates to the severity of the bowel inflammation.[15]

Virulence properties[edit]

Enteric E. coli (EC) are classified on the basis of serological characteristics and virulence properties.[11] Virotypes include:

NameHostsDescription
Enterotoxigenic
E. coli (ETEC)
causative agent of diarrhea (without fever) in humans, pigs, sheep, goats, cattle, dogs, and horsesETEC uses fimbrial adhesins (projections from the bacterial cell surface) to bind enterocyte cells 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.
  • 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 noninvasive, and they do not leave the intestinal lumen. ETEC is the leading bacterial cause of diarrhoea in children in the developing world, as well as the most common cause of traveler's diarrhoea. Each year, ETEC causes more than 200 million cases of diarrhoea and 380,000 deaths, mostly in children in developing countries.[16]

Enteropathogenic E. coli (EPEC)causative agent of diarrhoea in humans, rabbits, dogs, cats and horsesLike ETEC, EPEC also causes diarrhoea, but the molecular mechanisms of colonization and aetiology are different. EPEC lack fimbriae, ST and LT toxins, but they use 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 possess 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)
found only in humansEIEC infection causes a syndrome that is identical to shigellosis, with profuse diarrhoea and high fever.
Enterohemorrhagic
E. coli
(EHEC)
found in humans, cattle, and goatsThe most infamous member of this virotype is strain O157:H7, which causes bloody diarrhoea and no fever. EHEC can cause hemolytic-uremic syndrome and sudden kidney failure. It uses bacterial fimbriae for attachment (E. coli common pilus, ECP),[17] is moderately invasive and possesses a phage-encoded shiga toxin that can elicit an intense inflammatory response.
Enteroaggregative
E. coli
(EAEC)
found only in humansSo named because they have fimbriae which aggregate tissue culture cells, EAEC bind to the intestinal mucosa to cause watery diarrhoea without fever. EAEC are noninvasive. They produce a hemolysin and an ST enterotoxin similar to that of ETEC.

Epidemiology of gastrointestinal infection[edit]

Transmission of pathogenic E. coli often occurs via faecal–oral transmission.[18][19][20] Common routes of transmission include: unhygienic food preparation,[19] farm contamination due to manure fertilization,[21] irrigation of crops with contaminated greywater or raw sewage,[22] feral pigs on cropland,[23] or direct consumption of sewage-contaminated water.[24] Dairy and beef cattle are primary reservoirs of E. coli O157:H7,[25] and they can carry it asymptomatically and shed it in their faeces.[25] Food products associated with E. coli outbreaks include cucumber,[26] raw ground beef,[27] raw seed sprouts or spinach,[21] raw milk, unpasteurized juice, unpasteurized cheese and foods contaminated by infected food workers via faecal–oral route.[19]

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

Shiga toxin-producing E. coli (STEC), specifically serotype O157:H7, have also been transmitted by flies,[28][29][30] as well as direct contact with farm animals,[31][32] petting zoo animals,[33] and airborne particles found in animal-rearing environments.[34]

Urinary tract infection[edit]

E. coli bacteria

Uropathogenic E. coli (UPEC) is responsible for approximately 90% of urinary tract infections (UTI) seen in individuals with ordinary anatomy.[11] In ascending infections, fecal bacteria colonize the urethra and spread up the urinary tract to the bladder as well as to the kidneys (causing pyelonephritis),[35] or the prostate in males. Because women have a shorter urethra than men, they are 14 times more likely to suffer from an ascending UTI.[11]

Uropathogenic E. coli use P fimbriae (pyelonephritis-associated pili) to bind urinary tract urothelial cells and colonize the bladder. These adhesins specifically bind D-galactose-D-galactose moieties on the P blood-group antigen of erythrocytes and uroepithelial cells.[11] Approximately 1% of the human population lacks this receptor,[citation needed] and its presence or absence dictates an individual's susceptibility or non-susceptibility, respectively, to E. coli urinary tract infections. Uropathogenic E. coli produce alpha- and beta-hemolysins, which cause lysis of urinary tract cells.

Another virulence factor commonly present in UPEC is the Dr family of adhesins, which are particularly associated with cystitis and pregnancy-associated pyelonephritis.[36] The Dr adhesins bind Dr blood group antigen (Dra) which is present on decay accelerating factor (DAF) on erythrocytes and other cell types. There, the Dr adhesins induce the development of long cellular extensions that wrap around the bacteria, accompanied by the activation of several signal transduction cascades, including activation of PI-3 kinase.[36]

UPEC can evade the body's innate immune defences (e.g. the complement system) by invading superficial umbrella cells to form intracellular bacterial communities (IBCs).[37] They also have the ability to form K antigen, capsular polysaccharides that contribute to biofilm formation. Biofilm-producing E. coli are recalcitrant to immune factors and antibiotic therapy, and are often responsible for chronic urinary tract infections.[38] K antigen-producing E. coli infections are commonly found in the upper urinary tract.[11]

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

Neonatal meningitis(NMEC)[edit]

It is produced by a serotype of Escherichia coli that contains a capsular antigen called K1. The colonisation of the newborn's intestines with these stems, that are present in the mother's vagina, lead to bacteraemia, which leads to meningitis.[citation needed] And because of the absence of the IgM antibodies from the mother (these do not cross the placenta because FcRn only mediates the transfer of IgG), plus the fact that the body recognises as self the K1 antigen, as it resembles the cerebral glicopeptides, this leads to a severe meningitis in the neonates.

Involvement in cancer[edit]

There are some E. coli strains that contain a polyketide synthase genomic island (pks) whose function is to encode a multi-enzymatic machinery that produces a genotoxic substance, named colibactin. This substance can promote tumorgenesis by harming DNA. However, the mucosal barrier prevents E. coli from reaching the surface of enterocytes. Only when some inflammatory lesion co-occurs with E. coli infection the bacterium is able to inject colibactin to enterocytes inducing tumorogenesis.[39]

Animal diseases[edit]

In animals, virulent strains of E. coli are responsible of a variety of diseases, among others septicemia and diarrhea in newborn calves, acute mastitis in dairy cows, colibacillosis also associated with chronic respiratory disease with Mycoplasma where it causes perihepatitis, pericarditis, septicaemic lungs, peritonitis etc. in poultry, and Alabama rot in dogs.

Most of the serotypes isolated from poultry are pathogenic only for birds. So avian sources of E. coli do not seem to be important sources of infections in other animals.[40]

Laboratory diagnosis[edit]

In stool samples, microscopy will show gram-negative rods, with no particular cell arrangement. Then, either MacConkey agar or EMB agar (or both) are inoculated with the stool. On MacConkey agar, deep red colonies are produced, as the organism is lactose-positive, and fermentation of this sugar will cause the medium's pH to drop, leading to darkening of the medium. Growth on EMB agar produces black colonies with a greenish-black metallic sheen. This is diagnostic of E. coli. The organism is also lysine positive, and grows on TSI slant with a (A/A/g+/H2S-) profile. Also, IMViC is {+ + – -} for E. coli; as it is indole-positive (red ring) and methyl red-positive (bright red), but VP-negative (no change-colourless) and citrate-negative (no change-green colour). Tests for toxin production can use mammalian cells in tissue culture, which are rapidly killed by shiga toxin. Although sensitive and very specific, this method is slow and expensive.[41]

Typically, diagnosis has been done by culturing on sorbitol-MacConkey medium and then using typing antiserum. However, current latex assays and some typing antisera have shown cross reactions with non-E. coli O157 colonies. Furthermore, not all E. coli O157 strains associated with HUS are nonsorbitol fermentors.

The Council of State and Territorial Epidemiologists recommend that clinical laboratories screen at least all bloody stools for this pathogen. The U.S. Centers for Disease Control and Prevention recommend that "all stools submitted for routine testing from patients with acute community-acquired diarrhea (regardless of patient age, season of the year, or presence or absence of blood in the stool) be simultaneously cultured for E. coli O157:H7 (O157 STEC) and tested with an assay that detects Shiga toxins to detect non-O157 STEC".[42][43]

Antibiotic therapy and resistance[edit]

Main article: Antibiotic resistance

Bacterial infections are usually treated with antibiotics. However, the antibiotic sensitivities of different strains of E. coli vary widely. As gram-negative organisms, E. coli are 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 semisynthetic penicillins, many cephalosporins, carbapenems, aztreonam, trimethoprim-sulfamethoxazole, ciprofloxacin, nitrofurantoin and the aminoglycosides.

Antibiotic resistance is a growing problem. Some of this is due to overuse of antibiotics in humans, but some of it is probably due to the use of antibiotics as growth promoters in animal feeds.[44] A study published in the journal Science in August 2007 found 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," a finding which may have significance for the study and management of bacterial antibiotic resistance.[45]

Antibiotic-resistant E. coli may also pass on the genes responsible for antibiotic resistance to other species of bacteria, such as Staphylococcus aureus, through a process called horizontal gene transfer. E. coli bacteria often carry multiple drug-resistance plasmids, and under stress, readily transfer those plasmids to other species. Indeed, 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.[46]

Beta-lactamase strains[edit]

Resistance to beta-lactam antibiotics has become a particular problem in recent decades, as strains of bacteria that produce extended-spectrum beta-lactamases have become more common.[47] These beta-lactamase enzymes make many, if not all, of the penicillins and cephalosporins ineffective as therapy. Extended-spectrum beta-lactamase–producing E. coli (ESBL E. coli) are highly resistant to an array of antibiotics, and infections by these strains are difficult to treat. In many instances, only two oral antibiotics and a very limited group of intravenous antibiotics remain effective. In 2009, a gene called New Delhi metallo-beta-lactamase (shortened NDM-1) that even gives resistance to intravenous antibiotic carbapenem, were discovered in India and Pakistan on E. coli bacteria.

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.[48] Susceptibility testing should guide treatment in all infections in which the organism can be isolated for culture.

Phage therapy[edit]

Phage therapy—viruses that specifically target pathogenic bacteria—has been developed over the last 80 years, primarily in the former Soviet Union, where it was used to prevent diarrhoea caused by E. coli.[49] Presently, phage therapy for humans is available only at the Phage Therapy Center in the Republic of Georgia and in Poland.[50] However, on January 2, 2007, the United States FDA gave Omnilytics approval to apply its E. coli O157:H7 killing phage in a mist, spray or wash on live animals that will be slaughtered for human consumption.[51] The enterobacteria phage T4, a highly studied phage, targets E. coli for infection.

Vaccination[edit]

Researchers have actively been working to develop safe, effective vaccines to lower the worldwide incidence of E. coli infection.[52] 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 it was safe for adults.[53] A phase III clinical trial to verify the large-scale efficacy of the treatment is planned.[53]

In 2006, Fort Dodge Animal Health (Wyeth) introduced an effective, live, attenuated vaccine to control airsacculitis and peritonitis in chickens. The vaccine is a genetically modified avirulent vaccine that has demonstrated protection against O78 and untypeable strains.[54]

In January 2007, the Canadian biopharmaceutical company Bioniche announced it has developed a cattle vaccine which reduces the number of O157:H7 shed in manure by a factor of 1000, to about 1000 pathogenic bacteria per gram of manure.[55][56][57]

In April 2009, a Michigan State University researcher announced he had developed a working vaccine for a strain of E. coli. Dr. Mahdi Saeed, Professor of epidemiology and infectious disease in MSU's colleges of Veterinary Medicine and Human Medicine, has applied for a patent for his discovery and has made contact with pharmaceutical companies for commercial production.[58]

See also[edit]

References[edit]

  1. ^ "Escherichia coli O157:H7". CDC Division of Bacterial and Mycotic Diseases. Retrieved 2011-04-19. 
  2. ^ Vogt RL, Dippold L (2005). "Escherichia coli O157:H7 outbreak associated with consumption of ground beef, June–July 2002". Public Health Rep 120 (2): 174–8. PMC 1497708. PMID 15842119. 
  3. ^ Bentley R, Meganathan R (1 September 1982). "Biosynthesis of vitamin K (menaquinone) in bacteria". Microbiol. Rev. 46 (3): 241–80. PMC 281544. PMID 6127606. 
  4. ^ Hudault S, Guignot J, Servin AL (July 2001). "Escherichia coli strains colonising the gastrointestinal tract protect germfree mice against Salmonella typhimurium infection". Gut 49 (1): 47–55. doi:10.1136/gut.49.1.47. PMC 1728375. PMID 11413110. 
  5. ^ Reid G, Howard J, Gan BS (September 2001). "Can bacterial interference prevent infection?". Trends Microbiol. 9 (9): 424–428. doi:10.1016/S0966-842X(01)02132-1. PMID 11553454. 
  6. ^ Eckburg PB, Bik EM, Bernstein CN, Purdom E, Dethlefsen L et al. (2005). "Diversity of the human intestinal microbial flora". Science 308 (5728): 1635–1638. doi:10.1126/science.1110591. PMC 1395357. PMID 15831718. 
  7. ^ a b Feng P, Weagant S, Grant, M (2002-09-01). "Enumeration of Escherichia coli and the Coliform Bacteria". Bacteriological Analytical Manual (8th ed.). FDA/Center for Food Safety & Applied Nutrition. Retrieved 2007-01-25. 
  8. ^ Thompson, Andrea (2007-06-04). "E. coli Thrives in Beach Sands". Live Science. Retrieved 2007-12-03. 
  9. ^ "Escherichia". Taxonomy Browser. NCBI. Retrieved 2007-11-30. 
  10. ^ a b c d e f g Don J. Brenner, Noel R. Krieg, James T. Staley (July 26, 2005) [1984(Williams & Wilkins)]. George M. Garrity, ed. The Gammaproteobacteria. Bergey's Manual of Systematic Bacteriology 2B (2nd ed.). New York: Springer. p. 1108. ISBN 978-0-387-24144-9. British Library no. GBA561951. 
  11. ^ a b c d e f Todar, K. "Pathogenic E. coli". Online Textbook of Bacteriology. University of Wisconsin–Madison Department of Bacteriology. Retrieved 2007-11-30. 
  12. ^ Tauschek M, Gorrell R, Robins-Browne RM,. "Identification of a protein secretory pathway for the secretion of heat-labile enterotoxin by an enterotoxigenic strain of Escherichia coli". PNAS 99 (10): 7066–71. doi:10.1073/pnas.092152899. PMC 124529. PMID 12011463. 
  13. ^ Wong CS, Jelacic S, Habeeb RL, et al. (29 June 2000). "The risk of the hemolytic-uremic syndrome after antibiotic treatment of Escherichia coli O157:H7 infections.". N Engl J Med 342 (26): 1930–6. doi:10.1056/NEJM200006293422601. PMC 3659814. PMID 10874060. 
  14. ^ Rolhion N, Darfeuille-Michaud A (2007). "Adherent-invasive Escherichia coli in inflammatory bowel disease". Inflamm. Bowel Dis. 13 (10): 1277–1283. doi:10.1002/ibd.20176. PMID 17476674. 
  15. ^ Baumgart M, Dogan B, Rishniw M et al. (2007). "Culture independent analysis of ileal mucosa reveals a selective increase in invasive Escherichia coli of novel phylogeny relative to depletion of Clostridiales in Crohn's disease involving the ileum". ISME J 1 (5): 403–418. doi:10.1038/ismej.2007.52. PMID 18043660. 
  16. ^ "World Health Organization. Enterotoxigenic ''Escherichia coli'' (ETEC)". Who.int. 2010-12-08. Retrieved 2011-06-05. 
  17. ^ Rendón, M. A. et al. (2007). "Commensal and pathogenic Escherichia coli use a common pilus adherence factor for epithelial cell colonization". PNAS 104 (25): 10637–10642. doi:10.1073/pnas.0704104104. PMC 1890562. PMID 17563352. 
  18. ^ Evans Jr., Doyle J.; Dolores G. Evans. "Escherichia Coli". Medical Microbiology, 4th edition. The University of Texas Medical Branch at Galveston. Archived from the original on 2007-11-02. Retrieved 2007-12-02. 
  19. ^ a b c d "Retail Establishments; Annex 3 – Hazard Analysis". Managing Food Safety: A Manual for the Voluntary Use of HACCP Principles for Operators of Food Service and Retail Establishments. U.S. Department of Health and Human Services Food and Drug Administration Center for Food Safety and Applied Nutrition. April 2006. Archived from the original on 2007-06-07. Retrieved 2007-12-02. 
  20. ^ Gehlbach, S.H.; J.N. MacCormack, B.M. Drake, W.V. Thompson (April 1973). "Spread of disease by fecal-oral route in day nurseries". Health Service Reports 88 (4): 320–322. doi:10.2307/4594788. JSTOR 4594788. PMC 1616047. PMID 4574421. 
  21. ^ a b Sabin Russell (October 13, 2006). "Spinach E. coli linked to cattle; Manure on pasture had same strain as bacteria in outbreak". San Francisco Chronicle. Retrieved 2007-12-02. 
  22. ^ Heaton JC, Jones K (March 2008). "Microbial contamination of fruit and vegetables and the behaviour of enteropathogens in the phyllosphere: a review". J. Appl. Microbiol. 104 (3): 613–626. doi:10.1111/j.1365-2672.2007.03587.x. PMID 17927745. 
  23. ^ Thomas R. DeGregori (2007-08-17). "CGFI: Maddening Media Misinformation on Biotech and Industrial Agriculture". Retrieved 2007-12-08. 
  24. ^ Chalmers, R.M.; H. Aird, F.J. Bolton (2000). "Waterborne Escherichia coli O157". Society for Applied Microbiology Symposium Series (29): 124S–132S. PMID 10880187. 
  25. ^ a b Bach, S.J.; T.A. McAllister, D.M. Veira, V.P.J. Gannon, and R.A. Holley (2002). "Transmission and control of Escherichia coli O157:H7". Canadian Journal of Animal Science 82 (4): 475–490. doi:10.4141/A02-021. 
  26. ^ "Germany: Ten die from E.coli-infected cucumbers". BBC. 28 May 2011. Retrieved 28 May 2011. 
  27. ^ Institute of Medicine of the National Academies; Committee on the Review of the USDA E. coli O157:H7 Farm-to-Table Process Risk Assessment, Board on Health Promotion and Disease Prevention Food and Nutrition Board, Institute of Medicine of the National Academies. (2002). Escherichia coli O157:H7 in Ground Beef: Review of a Draft Risk Assessment. Washington, D.C.: The National Academies Press. ISBN 0-309-08627-2. 
  28. ^ Szalanski A, Owens C, McKay T, Steelman C (2004). "Detection of Campylobacter and Escherichia coli O157:H7 from filth flies by polymerase chain reaction". Med Vet Entomol 18 (3): 241–6. doi:10.1111/j.0269-283X.2004.00502.x. PMID 15347391. 
  29. ^ Sela S, Nestel D, Pinto R, Nemny-Lavy E, Bar-Joseph M (2005). "Mediterranean fruit fly as a potential vector of bacterial pathogens". Appl Environ Microbiol 71 (7): 4052–6. doi:10.1128/AEM.71.7.4052-4056.2005. PMC 1169043. PMID 16000820. 
  30. ^ Alam M, Zurek L (2004). "Association of Escherichia coli O157:H7 with houseflies on a cattle farm". Appl Environ Microbiol 70 (12): 7578–80. doi:10.1128/AEM.70.12.7578-7580.2004. PMC 535191. PMID 15574966. 
  31. ^ Rahn, K.; S.A. Renwick, R.P. Johnson, J.B. Wilson, R.C. Clarke, D. Alves, S.A. McEwen, H. Lior, J. Spika (April 1998). "Follow-up study of verocytotoxigenic Escherichia coli infection in dairy farm families". Journal of Infectious Disease 177 (4): 1139–1139. doi:10.1086/517394. PMID 9535003. 
  32. ^ Trevena, W.B.; G.A Willshaw, T. Cheasty, G. Domingue, C. Wray (December 1999). "Transmission of Vero cytotoxin producing Escherichia coli O157 infection from farm animals to humans in Cornwall and west Devon". Community Disease and Public Health 2 (4): 263–8. PMID 10598383. 
  33. ^ Heuvelink, A.E.; C. van Heerwaarden, J.T. Zwartkruis-Nahuis, R. van Oosterom, K. Edink, Y.T. van Duynhoven and E. de Boer (October 2002). "Escherichia coli O157 infection associated with a petting zoo". Epidemiology and Infection 129 (2): 295–302. doi:10.1017/S095026880200732X. PMC 2869888. PMID 12403105. 
  34. ^ Varma, J.K.; K.D. Greene, M.E. Reller, S.M. DeLong, J. Trottier, S.F. Nowicki, M. DiOrio, E.M. Koch, T.L. Bannerman, S.T. York, M.A. Lambert-Fair, J.G. Wells, P.S. Mead (November 26, 2003). "An outbreak of Escherichia coli O157 infection following exposure to a contaminated building". JAMA 290 (20): 2709–2712. doi:10.1001/jama.290.20.2709. PMID 14645313. 
  35. ^ Nicolle LE (February 2008). "Uncomplicated urinary tract infection in adults including uncomplicated pyelonephritis". Urol. Clin. North Am. 35 (1): 1–12. doi:10.1016/j.ucl.2007.09.004. PMID 18061019. 
  36. ^ a b Identified Virulence Factors of UPEC : Adherence, State Key Laboratory for Moleclular Virology and Genetic Engineering, Beijing. Retrieved July 2011
  37. ^ Justice S, Hunstad D, Seed P, Hultgren S (2006). "Filamentation by Escherichia coli subverts innate defenses during urinary tract infection". Proc Natl Acad Sci U S A 103 (52): 19884–9. doi:10.1073/pnas.0606329104. PMC 1750882. PMID 17172451. 
  38. ^ Ehrlich G, Hu F, Shen K, Stoodley P, Post J (August 2005). "Bacterial plurality as a general mechanism driving persistence in chronic infections". Clin Orthop Relat Res (437): 20–4. doi:10.1097/00003086-200508000-00005. PMC 1351326. PMID 16056021. 
  39. ^ Arthur, Janelle C.; et al. (5 October 2012). "Intestinal Inflammation Targets Cancer-Inducing Activity of the Microbiota". Science 338. doi:10.1126/science.1224820. 
  40. ^ W.B. Gross (1978), Colibacillosis, in "Diseases of poultry", ed. by M.S. Hofstad, Iowa State University Press, Ames, Iowa, USA; 8th ed. ISBN 0-8138-0430-2, p. 270
  41. ^ Paton JC, Paton AW (1 July 1998). "Pathogenesis and diagnosis of Shiga toxin-producing Escherichia coli infections". Clin. Microbiol. Rev. 11 (3): 450–79. PMC 88891. PMID 9665978. 
  42. ^ "Importance of Culture Confirmation of Shiga Toxin-producing Escherichia coli Infection as Illustrated by Outbreaks of Gastroenteritis --- New York and North Carolina, 2005". MMWR. CDC. Retrieved 19 July 2011. 
  43. ^ "Recommendations for Diagnosis of Shiga Toxin--Producing Escherichia coli Infections by Clinical Laboratories". MMWR Recommendations and Reports. CDC (USA). Retrieved 19 July 2011. 
  44. ^ Johnson J, Kuskowski M, Menard M, Gajewski A, Xercavins M, Garau J (2006). "Similarity between human and chicken Escherichia coli isolates in relation to ciprofloxacin resistance status". J Infect Dis 194 (1): 71–8. doi:10.1086/504921. PMID 16741884. 
  45. ^ Perfeito, Lília; Fernandes, Lisete; Mota, Catarina; Gordo, Isabel (2007). "Adaptive Mutations in Bacteria: High Rate and Small Effects". Science 317 (5839): 813–815. doi:10.1126/science.1142284. 
  46. ^ Salyers AA, Gupta A, Wang Y (2004). "Human intestinal bacteria as reservoirs for antibiotic resistance genes". Trends Microbiol. 12 (9): 412–6. doi:10.1016/j.tim.2004.07.004. PMID 15337162. 
  47. ^ Paterson DL, Bonomo RA (2005). "Extended-spectrum beta-lactamases: a clinical update". Clin. Microbiol. Rev. 18 (4): 657–86. doi:10.1128/CMR.18.4.657-686.2005. PMC 1265908. PMID 16223952. 
  48. ^ "HPA Press Statement: Infections caused by ESBL-producing E. coli". 
  49. ^ "Therapeutic use of bacteriophages in bacterial infections". Polish Academy of Sciences. 
  50. ^ "Medical conditions treated with phage therapy". Phage Therapy Center. 
  51. ^ "OmniLytics Announces USDA/FSIS Approval for Bacteriophage Treatment of E. coli O157:H7 on Livestock". OmniLytics. 
  52. ^ Girard M, Steele D, Chaignat C, Kieny M (2006). "A review of vaccine research and development: human enteric infections". Vaccine 24 (15): 2732–50. doi:10.1016/j.vaccine.2005.10.014. PMID 16483695. 
  53. ^ a b Ahmed A, Li J, Shiloach Y, Robbins J, Szu S (2006). "Safety and immunogenicity of Escherichia coli O157 O-specific polysaccharide conjugate vaccine in 2-5-year-old children". J Infect Dis 193 (4): 515–21. doi:10.1086/499821. PMID 16425130. 
  54. ^ [1][dead link]
  55. ^ Pearson H (2007). "The dark side of E. coli". Nature 445 (7123): 8–9. doi:10.1038/445008a. PMID 17203031. 
  56. ^ "New cattle vaccine controls E. coli infections". Canada AM. 2007-01-11. Retrieved 2007-02-08. 
  57. ^ "Canadian Research Collaboration Produces World's First Food Safety Vaccine: Against E. coli O157:H7" (Press release). Bioniche Life Sciences Inc. 2007-01-10. Retrieved 2007-02-08. 
  58. ^ "Researchers develop E. coli vaccine". Physorg.com. Retrieved 2011-06-05. 
Creative Commons Attribution Share Alike 3.0 (CC BY-SA 3.0)

Source: Wikipedia

Unreviewed

Article rating from 0 people

Default rating: 2.5 of 5

Escherichia coli O104:H21

Escherichia coli O104:H21 is a rare serotype of Escherichia coli, a species of bacteria that lives in the lower intestines of mammals.[1] The presence of many serotypes of E. coli in animals is beneficial or does not cause disease in animals. However, some serotypes of E. coli have been recognized as pathogenic to humans, e.g. E. coli O157:H7, E. coli O121 and E. coli O104:H21.

Contents

History

E. coli O104:H21 was discovered in 1982, when it caused an outbreak of severe bloody diarrhea. It had infected hamburgers, and those affected had eaten these hamburgers not fully cooked.[2]

An outbreak of E. coli responsible for at least 22 deaths in Northern Europe in May 2011 was reported to be caused by another O104 strain, Escherichia coli O104:H4.

Effects

E. coli O104:H21 can cause outbreak of infection similar to that caused by E. coli O157:H7, the most common shiga-like toxin-producing E. coli (SLTEC). SLTECs are the most well-known causes of gastrointestinal illness and diarrhea.[3]

Treatment

The body usually rids itself of harmful E. coli O104:H21 on its own within 5 to 10 days. Antibiotics should not be used, and neither should antidiarrheal agents such as loperamide.[2]

See also

References

  1. ^ http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5602a2.htm Laboratory-Confirmed Non-O157 Shiga Toxin Producing E. Coli, Centers for Disease Control and Prevention, accessed March 16, 2007
  2. ^ a b http://www.cdc.gov/ncidod/dbmd/diseaseinfo/escherichiacoli_g.htm#What%20is%20Escherichia%20coli%20O157:H7 Centers for Disease Control and Prevention, Last Accessed August 1, 2007
  3. ^ http://www.cdc.gov/mmwr/preview/mmwrhtml/00038146.htm Outbreak of Acute Gastroenteritis Attributable to Escherichia coli Serotype O104:H21, Centers for Disease Control and Prevention, accessed July 31, 2007
Creative Commons Attribution Share Alike 3.0 (CC BY-SA 3.0)

Source: Wikipedia

Unreviewed

Article rating from 0 people

Default rating: 2.5 of 5

Names and Taxonomy

Taxonomy

Taxonomic Hierarchy

Domain: Bacteria

Phylum: Proteobacteria

Class: Gammaproteobacteria

Order: Enterobacteriales 

Family: Enterobacteriaceae 

Genus: Escherichia 

Species: E. coli

Creative Commons Attribution 3.0 (CC BY 3.0)

© ColeDewey

Supplier: ColeDewey

Unreviewed

Article rating from 0 people

Default rating: 2.5 of 5

Disclaimer

EOL content is automatically assembled from many different content providers. As a result, from time to time you may find pages on EOL that are confusing.

To request an improvement, please leave a comment on the page. Thank you!