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What makes E. coli yellowish?

What makes E. coli yellowish?


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LB, TB media, and yeast extract are also yellow but at the heart of the question. What chemical(s) make E. coli yellow?


I think of E. coli being more white than yellow. When you compare E. coli and S. aureus on an agar plate, the Staph colonies have a much more distinctive yellow tint. The yellow tint in Staph colonies is due to staphyloxanthin, a carotenoid pigment.


You will be surprised that when describing the colonial morphology of E. coli on a Blood agar plate, the word choice for colour is "grey". I believe that user leonardo up there had a very good explanation about this "yellowish colour" question.


Bobthejoe's comment is the best answer so far. Despite many other types of bacterial colonies being "more" yellow than E. coli, E. coli is definitely not white.

Flavins, especially riboflavins, are the predominant compound responsible for this coloration.


E. Coli Genome Reported: Milestone of Modern Biology Emerges From Laboratory of Genetics

A team of scientists headed by Frederick Blattner of the E. coli Genome Project in the Laboratory of Genetics at UW–Madison has determined the complete genome sequence of the E. coli bacterium, it was reported in the Sept. 5 issue of the journal Science.

A genome is the sum total of the genes of an organism. Genes are encoded in the sequence of chemical base pairs that make up the intertwining strands of DNA. In the case of E. coli, a total of 4,403 genes have been identified in the 4,639,221 base pairs of DNA sequenced by the Wisconsin team. Of these, one-third are of completely unknown function.

E. coli holds a unique place in modern biology. It is arguably the single most studied cell in all of science. Humans have about 25 times as many genes as E. coli, but in the future a similar complete analysis will be possible for human DNA. For this reason E. coli is considered a model organism in the Human Genome Initiative of the National Institutes of Health (NIH).

For more than 70 years, Escherichia coli has been a mainstay of basic biology, and recent developments in biotechnology and genetic engineering have depended heavily on it. Related strains of E. coli are also responsible for several human diseases. Although not the first bacterial genome to be completed, E. coli is by far the most complex and the most eagerly awaited by scientists around the world.

“Determination of the complete inventory of the genes of organisms is one of the holy grails of biology, analogous to development of the periodic table of the elements in chemistry,” said Blattner. “Once they are all known and relationships between them become evident, a classification system for understanding the basic functions of life can be erected.”

E. coli’s natural habitat is the lower intestinal tract of animals, including humans. Originally isolated in 1922 from a convalescent diphtheria patient, the strain of E. coli sequenced by Blattner’s team rose to prominence as an experimental organism in 1945 when it was used in the discovery of spontaneous gene transfer or bacterial sex. As a result, the strain, known as K-12, was universally adopted for fundamental work in biochemistry, genetics and physiology. In recent years, it has become the workhorse of biotechnology and is used as a living factory to produce human insulin and other medicines.

The most important result of the work reported today is the sequence itself, said Blattner. In January, the data were made freely available through on-line databases such as GenBank to scientists worldwide. The E. coli genome is a huge one, and required an additional nine months to describe in detail in Science. With more than 4.6 million bases, it is two or three times bigger than other bacteria sequenced to date.

Sequencing of the base pairs that make up DNA is analogous to deciphering a language. It is done with the aid of specialized chemical analysis machines, but can only be accomplished with considerable human effort. More than 269 people – including many undergraduates getting their first taste of science – participated in the project at the UW–Madison.

The individual chemical bases that make up the genome correspond to the letters of the genetic alphabet which, grouped into words and paragraphs corresponding to genes, are read by the living cell as the instructions for assembly and function of all of life’s processes.

Knowledge of the genetic code, a major effort of modern biology, permits the scientist to translate the instructions for the purpose of understanding life processes, Blattner said. Knowing the precise order of the chemical base pairs for an entire genome allows the encoded life program to be read in its entirety leading, in principle, to a very complete level of understanding of physiological processes.

The report published in this issue of Science is a global analysis of the data collected by Blattner’s team in collaboration with Monica A. Riley of the Marine Biological Laboratories in Woods Hole, Mass., and Julio Collado-Vides of the University of Mexico at Cuernavaca.

The report, first and foremost, represents a record of the genes that make up the genome of the organism, and the establishment, where possible, of their functions. A surprising number of the genes, Blattner said, are new.

The work also details the similarity between every gene of E. coli and every gene of every other completely sequenced organism. The comparison, according to Blattner, shows that some genes appear commonly throughout nature while others are unique to E. coli. Such information is essential to any understanding of how E. coli and other bacteria have evolved, and what genes are required at a minimum to create life.

In addition to the base order of the chemical building blocks that make up the E. coli genome, and a better sense of its evolution and relationship to other organisms, the work of Blattner’s team has yielded a lode of new information about the organization of E. coli genes and how the information stored there is distributed.

It was noticed, too, that some of the DNA may have been added within the recent evolutionary history of the microbe. This immigrant DNA, said Blattner, is seemingly related to the genes of bacteria that cause disease, fueling speculation that the K-12 strain of E. coli has relics of a pathogenic past or, alternatively, is a pathogen waiting to happen.

The E. coli strain used in the Wisconsin study does not cause disease, but related strains are toxic and have been implicated in an increasing number of human food poisonings from products ranging from ground beef to unpasteurized apple juice to fecally contaminated lettuce. With the K-12 E. coli genome in hand, Blattner said it will soon be possible to make a gene by gene comparison with its pathogenic relatives and illuminate genes that govern the toxic nature of the bacteria.

The sequencing of the E. coli genome, said Blattner, was a necessary precursor to the sequencing of the human genome, now underway as part of the Human Genome Project under the direction of the National Human Genome Research Institute (NHGRI) of NIH. When scientists achieve this monumental goal, they will begin the daunting task of reading and understanding all of our protein-coding genes. They will accomplish this task, in part, by searching databases to find conserved biological motifs, first elucidated using simple model organisms like bacteria, yeast, worms and flies. By decoding the human genome, scientists can begin to decipher the genetic aspects of all disease, leading to improved treatments and even cures.

The NHGRI, a component of NIH, is a major partner in the Human Genome Project, the international research effort to map the estimated 50,000 to 100,000 genes and to read the complete set of genetic instructions encoded in human DNA. NHGRI also supports research on the application of genome technologies to the study of inherited disease, as well as the ethical, legal and social implications of this research. While primary funding for E. coli work came from the NHGRI, critical equipment was provided by the Division of Research Resources of the NIH. Substantial remodeling funds were provided to create the E. coli Genome Center by the WISTAR program of the State of Wisconsin, and research support was also provided by Genome Therapeutics Inc., SmithKline Beecham Inc., Dnastar Inc., and IBM.


Contents

Type and morphology Edit

E. coli is a Gram-negative, facultative anaerobe (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 nonsporulating bacterium. [17] Cells are typically rod-shaped, and are about 2.0 μm long and 0.25–1.0 μm in diameter, with a cell volume of 0.6–0.7 μm 3 . [18] [19] [20]

E. coli stains Gram-negative because its cell wall is composed of a thin peptidoglycan layer and an outer membrane. During the staining process, E. coli picks up the color of the counterstain safranin and stains pink. The outer membrane surrounding the cell wall provides a barrier to certain antibiotics such that E. coli is not damaged by penicillin. [15]

Strains that possess flagella are motile. The flagella have a peritrichous arrangement. [21] It also attaches and effaces to the microvilli of the intestines via an adhesion molecule known as intimin. [22]

Metabolism Edit

E. coli can live on a wide variety of substrates and 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. [23]

In addition, E. coli's metabolism can be rewired to solely use CO2 as the source of carbon for biomass production. In other words, this obligate heterotroph's metabolism can be altered to display autotrophic capabilities by heterologously expressing carbon fixation genes as well as formate dehydrogenase and conducting laboratory evolution experiments. This may be done by using formate to reduce electron carriers and supply the ATP required in anabolic pathways inside of these synthetic autotrophs. [24]

E. coli have three native glycolytic pathways: EMPP, EDP, and OPPP. The EMPP employs ten enzymatic steps to yield two pyruvates, two ATP, and two NADH per glucose molecule while OPPP serves as an oxidation route for NADPH synthesis. Although the EDP is the more thermodynamically favorable of the three pathways, E. coli do not use the EDP for glucose metabolism, relying mainly on the EMPP and the OPPP. The EDP mainly remains inactive except for during growth with gluconate. [25]

Catabolite Repression Edit

When growing in the presence of a mixture of sugars, bacteria will often consume the sugars sequentially through a process known as catabolite repression. By repressing the expression of the genes involved in metabolizing the less preferred sugars, cells will usually first consume the sugar yielding the highest growth rate, followed by the sugar yielding the next highest growth rate, and so on. In doing so the cells ensure that their limited metabolic resources are being used to maximize the rate of growth. The well-used example of this with E. coli involves the growth of the bacterium on glucose and lactose, where E. coli will consume glucose before lactose. Catabolite repression has also been observed in E.coli in the presence of other non-glucose sugars, such as arabinose and xylose, sorbitol, rhamnose, and ribose. In E. coli, glucose catabolite repression is regulated by the phosphotransferase system, a multi-protein phosphorylation cascade that couples glucose uptake and metabolism. [26]

Culture growth Edit

Optimum growth of E. coli occurs at 37 °C (98.6 °F), but some laboratory strains can multiply at temperatures up to 49 °C (120 °F). [27] E. coli grows in a variety of defined laboratory media, such as lysogeny broth, or any medium that contains glucose, ammonium phosphate monobasic, sodium chloride, magnesium sulfate, potassium phosphate dibasic, and water. 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. [28] E. coli is classified as a facultative anaerobe. It uses oxygen when it is present and available. It can, however, continue to grow in the absence of oxygen using fermentation or anaerobic respiration. The ability to continue growing in the absence of oxygen is an advantage to bacteria because their survival is increased in environments where water predominates. [15]

Cell cycle Edit

The bacterial cell cycle is divided into three stages. The B period occurs between the completion of cell division and the beginning of DNA replication. The C period encompasses the time it takes to replicate the chromosomal DNA. The D period refers to the stage between the conclusion of DNA replication and the end of cell division. [29] The doubling rate of E. coli is higher when more nutrients are available. However, the length of the C and D periods do not change, even when the doubling time becomes less than the sum of the C and D periods. At the fastest growth rates, replication begins before the previous round of replication has completed, resulting in multiple replication forks along the DNA and overlapping cell cycles. [30]

The number of replication forks in fast growing E. coli typically follows 2n (n = 1, 2 or 3). This only happens if replication is initiated simultaneously from all origins of replications, and is referred to as synchronous replication. However, not all cells in a culture replicate synchronously. In this case cells do not have multiples of two replication forks. Replication initiation is then referred to being asynchronous. [31] However, asynchrony can be caused by mutations to for instance DnaA [31] or DnaA initiator-associating protein DiaA. [32]

Genetic adaptation Edit

E. coli and related bacteria possess the ability to transfer DNA via bacterial conjugation or transduction, which allows genetic material to spread horizontally through an existing population. The process of transduction, which uses the bacterial virus called a bacteriophage, [33] is where the spread of the gene encoding for the Shiga toxin from the Shigella bacteria to E. coli helped produce E. coli O157:H7, the Shiga toxin-producing strain of E. coli.

E. coli encompasses an enormous population of bacteria that exhibit a very high degree of both genetic and phenotypic diversity. Genome sequencing of many 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, [34] and E. coli remains one of the most diverse bacterial species: only 20% of the genes in a typical E. coli genome is shared among all strains. [35]

In fact, from the more constructive point of view, the members of genus Shigella (S. dysenteriae, S. flexneri, S. boydii, and S. sonnei) should be classified as E. coli strains, a phenomenon termed taxa in disguise. [36] 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 subgroup 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. [12] [13] 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). [37] It is, however, common to cite only the serogroup, i.e. the O-antigen. At present, about 190 serogroups are known. [38] The common laboratory strain has a mutation that prevents the formation of an O-antigen and is thus not typeable.

Genome plasticity and evolution 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. [39] 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 often self-limiting in healthy adults but is frequently lethal to children in the developing world. [40] More virulent strains, such as O157:H7, cause serious illness or death in the elderly, the very young, or the immunocompromised. [40] [41]

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. [42] This was followed by a split of an Escherichia 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. [43]

The long-term evolution experiments using E. coli, begun by Richard Lenski in 1988, have allowed direct observation of genome evolution over more than 65,000 generations in the laboratory. [44] For instance, E. coli typically do not have the ability to grow aerobically with citrate as a carbon source, which is used as a diagnostic criterion with which to differentiate E. coli from other, closely, related bacteria such as Salmonella. In this experiment, one population of E. coli unexpectedly evolved the ability to aerobically metabolize citrate, a major evolutionary shift with some hallmarks of microbial speciation.

In the microbial world, a relationship of predation can be established similar to that observed in the animal world. Considered, it has been seen that E. coli is the prey of multiple generalist predators, such as Myxococcus xanthus. In this predator-prey relationship, a parallel evolution of both species is observed through genomic and phenotypic modifications, in the case of E. coli the modifications are modified in two aspects involved in their virulence such as mucoid production (excessive production of exoplasmic acid alginate ) and the suppression of the OmpT gene, producing in future generations a better adaptation of one of the species that is counteracted by the evolution of the other, following a co-evolutionary model demonstrated by the Red Queen hypothesis. [45]

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 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). [46] [47]

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 U5/41 T , [48] also known under the deposit names DSM 30083, [49] ATCC 11775, [50] and NCTC 9001, [51] which is pathogenic to chickens and has an O1:K1:H7 serotype. [52] However, in most studies, either O157:H7, K-12 MG1655, or K-12 W3110 were used as a representative E. coli. The genome of the type strain has only lately been sequenced. [48]

Phylogeny of E. coli strains Edit

Many 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. [53] [54] Particularly the use of whole genome sequences yields highly supported phylogenies. Based on such data, five subspecies of E. coli were distinguished. [48]

The link between phylogenetic distance ("relatedness") and pathology is small, [48] 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 E. albertii and E. fergusonii are outside this group. Indeed, all Shigella species were placed within a single subspecies of E. coli in a phylogenomic study that included the type strain, [48] and for this reason an according reclassification is difficult. 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).

E. coli S88 (O45:K1. Extracellular pathogenic)

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

E. coli (O19:H34. Extracellular pathogenic)

E. coli (O7:K1. Extracellular pathogenic)

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

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

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 B REL606 (O7. high competency molecular biology strain)

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

The first complete DNA sequence of an E. coli genome (laboratory strain K-12 derivative MG1655) was published in 1997. It is 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 about 40 years, many 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. [55]

More than three hundred complete genomic sequences of Escherichia and Shigella species are known. The genome sequence of the type strain of E. coli was added to this collection before 2014. [48] 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 around 80% of each genome can vary among isolates. [35] 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 pangenome) 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. [56]

Genes in E. coli are usually named by 4-letter acronyms that derive from their function (when known) and italicized. For instance, recA is named after its role in homologous recombination plus the letter A. Functionally related genes are named recB, recC, recD etc. The proteins are named by uppercase acronyms, e.g. RecA, RecB, etc. When the genome of E. coli was sequenced, all genes were numbered (more or less) in their order on the genome and abbreviated by b numbers, such as b2819 (= recD). The "b" names were created after Fred Blattner, who led the genome sequence effort. [55] Another numbering system was introduced with the sequence of another E. coli strain, W3110, which was sequenced in Japan and hence uses numbers starting by JW. (Japanese W3110), e.g. JW2787 (= recD). [57] Hence, recD = b2819 = JW2787. Note, however, that most databases have their own numbering system, e.g. the EcoGene database [58] uses EG10826 for recD. Finally, ECK numbers are specifically used for alleles in the MG1655 strain of E. coli K-12. [58] Complete lists of genes and their synonyms can be obtained from databases such as EcoGene or Uniprot.

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. [59] The 4,639,221–base pair sequence of Escherichia coli K-12 is presented. Of 4288 protein-coding genes annotated, 38 percent have no attributed function. Comparison with five other sequenced microbes reveals ubiquitous as well as narrowly distributed gene families many families of similar genes within E. coli are also evident. The largest family of paralogous proteins contains 80 ABC transporters. The genome as a whole is strikingly organized with respect to the local direction of replication guanines, oligonucleotides possibly related to replication and recombination, and most genes are so oriented. The genome also contains insertion sequence (IS) elements, phage remnants, and many other patches of unusual composition indicating genome plasticity through horizontal transfer. [55]

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. [60] A 2009 study found 5,993 interactions between proteins of the same E. coli strain, though these data showed little overlap with those of the 2006 publication. [61]

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. [62] This study also integrated genetic interactions and protein structures and mapped 458 interactions within 227 protein complexes.

E. coli belongs to a group of bacteria informally known as coliforms that are found in the gastrointestinal tract of warm-blooded animals. [63] E. coli normally colonizes an infant's gastrointestinal tract within 40 hours of birth, arriving with food or water or from the individuals handling the child. In the bowel, E. coli adheres to the mucus of the large intestine. It is the primary facultative anaerobe of the human gastrointestinal tract. [64] (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. [65]

Therapeutic use Edit

Due to the low cost and speed with which it can be grown and modified in laboratory settings, E. coli is a popular expression platform for the production of recombinant proteins used in therapeutics. One advantage to using E. coli over another expression platform is that E. coli naturally does not export many proteins into the periplasm, making it easier to recover a protein of interest without cross-contamination. [66] The E. coli K-12 strains and their derivatives (DH1, DH5α, MG1655, RV308 and W3110) are the strains most widely used by the biotechnology industry. [67] Nonpathogenic E. coli strain Nissle 1917 (EcN), (Mutaflor) and E. coli O83:K24:H31 (Colinfant) [68] [69] ) are used as probiotic agents in medicine, mainly for the treatment of various gastrointestinal diseases, [70] including inflammatory bowel disease. [71] It is thought that the EcN strain might impede the growth of opportunistic pathogens, including Salmonella and other coliform enteropathogens, through the production of microcin proteins the production of siderophores. [72]

Most E. coli strains do not cause disease, naturally living in the gut, [73] but virulent strains can cause gastroenteritis, urinary tract infections, neonatal meningitis, hemorrhagic colitis, and Crohn's disease. Common signs and symptoms include severe abdominal cramps, diarrhea, hemorrhagic colitis, vomiting, and sometimes fever. In rarer cases, virulent strains are also responsible for bowel necrosis (tissue death) and perforation without progressing to hemolytic-uremic syndrome, peritonitis, mastitis, sepsis, and Gram-negative pneumonia. Very young children are more susceptible to develop severe illness, such as hemolytic uremic syndrome however, healthy individuals of all ages are at risk to the severe consequences that may arise as a result of being infected with E. coli. [64] [74] [75] [76]

Some strains of E. coli, for example O157:H7, can produce Shiga toxin (classified as a bioterrorism agent). The Shiga toxin causes inflammatory responses in target cells of the gut, leaving behind lesions which result in the bloody diarrhea that is a symptom of a Shiga toxin-producing E. coli (STEC) infection. This toxin further causes premature destruction of the red blood cells, which then clog the body's filtering system, the kidneys, in some rare cases (usually in children and the elderly) causing hemolytic-uremic syndrome (HUS), which may lead to kidney failure and even death. Signs of hemolytic uremic syndrome include decreased frequency of urination, lethargy, and paleness of cheeks and inside the lower eyelids. In 25% of HUS patients, complications of nervous system occur, which in turn causes strokes. In addition, this strain causes the buildup of fluid (since the kidneys do not work), leading to edema around the lungs, legs, and arms. This increase in fluid buildup especially around the lungs impedes the functioning of the heart, causing an increase in blood pressure. [77] [22] [78] [79] [80] [75] [76]

Uropathogenic E. coli (UPEC) is one of the main causes of urinary tract infections. [81] It is part of the normal microbiota 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 bacterium into the male urethra, and in switching from anal to vaginal intercourse, the male can also introduce UPEC to the female urogenital system.

Enterotoxigenic E. coli (ETEC) is the most common cause of traveler's diarrhea, with as many as 840 million cases worldwide in developing countries each year. The bacteria, typically transmitted through contaminated food or drinking water, adheres to the intestinal lining, where it secretes either of two types of enterotoxins, leading to watery diarrhea. The rate and severity of infections are higher among children under the age of five, including as many as 380,000 deaths annually. [82]

In May 2011, one E. coli strain, O104:H4, was 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 also 15 other countries, including regions in North America. [83] On 30 June 2011, the German Bundesinstitut für Risikobewertung (BfR) (Federal Institute for Risk Assessment, a federal 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. [84]

Some studies have demonstrated an absence of E.coli in the gut flora of subjects with the metabolic disorder Phenylketonuria. It is hypothesized that the absence of these normal bacterium impairs the production of the key vitamins B2 (riboflavin) and K2 (menaquinone) - vitamins which are implicated in many physiological roles in humans such as cellular and bone metabolism - and so contributes to the disorder. [85]

Incubation period Edit

The time between ingesting the STEC bacteria and feeling sick is called the "incubation period". The incubation period is usually 3–4 days after the exposure, but may be as short as 1 day or as long as 10 days. The symptoms often begin slowly with mild belly pain or non-bloody diarrhea that worsens over several days. HUS, if it occurs, develops an average 7 days after the first symptoms, when the diarrhea is improving. [86]

Diagnosis Edit

Diagnosis of infectious diarrhea and identification of antimicrobial resistance is performed using a stool culture with subsequent antibiotic sensitivity testing. It requires a minimum of 2 days and maximum of several weeks to culture gastrointestinal pathogens. The sensitivity (true positive) and specificity (true negative) rates for stool culture vary by pathogen, although a number of human pathogens can not be cultured. For culture-positive samples, antimicrobial resistance testing takes an additional 12-24 hours to perform.

Current point of care molecular diagnostic tests can identify E. coli and antimicrobial resistance in the identified strains much faster than culture and sensitivity testing. Microarray-based platforms can identify specific pathogenic strains of E. coli and E. coli-specific AMR genes in two hours or less with high sensitivity and specificity, but the size of the test panel (i.e., total pathogens and antimicrobial resistance genes) is limited. Newer metagenomics-based infectious disease diagnostic platforms are currently being developed to overcome the various limitations of culture and all currently available molecular diagnostic technologies.

Treatment Edit

The mainstay of treatment is the assessment of dehydration and replacement of fluid and electrolytes. Administration of antibiotics has been shown to shorten the course of illness and duration of excretion of enterotoxigenic E. coli (ETEC) in adults in endemic areas and in traveller's diarrhea, though the rate of resistance to commonly used antibiotics is increasing and they are generally not recommended. [87] The antibiotic used depends upon susceptibility patterns in the particular geographical region. Currently, the antibiotics of choice are fluoroquinolones or azithromycin, with an emerging role for rifaximin. Oral rifaximin, a semisynthetic rifamycin derivative, is an effective and well-tolerated antibacterial for the management of adults with non-invasive traveller's diarrhea. Rifaximin was significantly more effective than placebo and no less effective than ciprofloxacin in reducing the duration of diarrhea. While rifaximin is effective in patients with E. coli-predominant traveller's diarrhea, it appears ineffective in patients infected with inflammatory or invasive enteropathogens. [88]

Prevention Edit

ETEC is the type of E. coli that most vaccine development efforts are focused on. Antibodies against the LT and major CFs of ETEC provide protection against LT-producing, ETEC-expressing homologous CFs. Oral inactivated vaccines consisting of toxin antigen and whole cells, i.e. the licensed recombinant cholera B subunit (rCTB)-WC cholera vaccine Dukoral, have been developed. There are currently no licensed vaccines for ETEC, though several are in various stages of development. [89] In different trials, the rCTB-WC cholera vaccine provided high (85–100%) short-term protection. An oral ETEC vaccine candidate consisting of rCTB and formalin inactivated E. coli bacteria expressing major CFs has been shown in clinical trials to be safe, immunogenic, and effective against severe diarrhoea in American travelers but not against ETEC diarrhoea in young children in Egypt. A modified ETEC vaccine consisting of recombinant E. coli strains over-expressing the major CFs and a more LT-like hybrid toxoid called LCTBA, are undergoing clinical testing. [90] [91]

Other proven prevention methods for E. coli transmission include handwashing and improved sanitation and drinking water, as transmission occurs through fecal contamination of food and water supplies. Additionally, thoroughly cooking meat and avoiding consumption of raw, unpasteurized beverages, such as juices and milk are other proven methods for preventing E.coli. Lastly, avoid cross-contamination of utensils and work spaces when preparing food. [92]

Because of its long history of laboratory culture and ease of manipulation, E. coli plays an important role in modern biological engineering and industrial microbiology. [93] 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. [94]

E. coli is a very versatile host for the production of heterologous proteins, [95] 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. [96]

Many proteins previously thought difficult or impossible to be expressed in E. coli in folded form have 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, [97] 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. [98] [99] [100]

Modified E. coli cells have been used in vaccine development, bioremediation, production of biofuels, [101] lighting, and production of immobilised enzymes. [95] [102]

Strain K-12 is a mutant form of E. coli that over-expresses the enzyme Alkaline Phosphatase (ALP). [103] The mutation arises due to a defect in the gene that constantly codes for the enzyme. A gene that is producing a product without any inhibition is said to have constitutive activity. This particular mutant form is used to isolate and purify the aforementioned enzyme. [103]

Strain OP50 of Escherichia coli is used for maintenance of Caenorhabditis elegans cultures.

Strain JM109 is a mutant form of E. coli that is recA and endA deficient. The strain can be utilized for blue/white screening when the cells carry the fertility factor episome [104] Lack of recA decreases the possibility of unwanted restriction of the DNA of interest and lack of endA inhibit plasmid DNA decomposition. Thus, JM109 is useful for cloning and expression systems.

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 laboratory strains lose their ability to form biofilms. [105] [106] These features protect wild-type strains from antibodies and other chemical attacks, but require a large expenditure of energy and material resources. E. coli is often used as a representative microorganism in the research of novel water treatment and sterilisation methods, including photocatalysis. By standard plate count methods, following sequential dilutions, and growth on agar gel plates, the concentration of viable organisms or CFUs (Colony Forming Units), in a known volume of treated water can be evaluated, allowing the comparative assessment of materials performance. [107]

In 1946, Joshua Lederberg and Edward Tatum first described the phenomenon known as bacterial conjugation using E. coli as a model bacterium, [108] and it remains the primary model to study conjugation. [109] E. coli was an integral part of the first experiments to understand phage genetics, [110] and early researchers, such as Seymour Benzer, used E. coli and phage T4 to understand the topography of gene structure. [111] Prior to Benzer's research, it was not known whether the gene was a linear structure, or if it had a branching pattern. [112]

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 [55]

From 2002 to 2010, a team at the Hungarian Academy of Science created a strain of Escherichia coli called MDS42, which is now sold by Scarab Genomics of Madison, WI under the name of "Clean Genome. E.coli", [113] where 15% of the genome of the parental strain (E. coli K-12 MG1655) were removed to aid in molecular biology efficiency, removing IS elements, pseudogenes and phages, resulting in better maintenance of plasmid-encoded toxic genes, which are often inactivated by transposons. [114] [115] [116] Biochemistry and replication machinery were not altered.

By evaluating the possible combination of nanotechnologies with landscape ecology, complex habitat landscapes can be generated with details at the nanoscale. [117] 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. [118]

In other studies, non-pathogenic E. coli has been used as a model microorganism towards understanding the effects of simulated microgravity (on Earth) on the same. [119] [120]

In 1885, the German-Austrian pediatrician Theodor Escherich discovered this organism in the feces of healthy individuals. He called it Bacterium coli commune because it is found in the colon. 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). [91] [121] [122]

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. [123] Following a revision of Bacterium, it was reclassified as Bacillus coli by Migula in 1895 [124] and later reclassified in the newly created genus Escherichia, named after its original discoverer. [125]

In 1996, the world's worst to date outbreak of E. coli food poisoning occurred in Wishaw, Scotland, killing 21 people. [126] This death toll was exceeded in 2011, when the 2011 Germany E. coli O104:H4 outbreak, linked to organic fenugreek sprouts, killed 53 people.


Contents

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]

In 1885, Theodor Escherich, a German pediatrician, first discovered this species in the feces of healthy individuals and called it Bacterium coli commune because 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]

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 DH10B (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 by Barbara Bachmann. [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 by Selman Waksman. [22]

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 used 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]

E. coli is frequently used as a model organism in microbiology studies. Cultivated strains (e.g. E. coli K-12) 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]

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.


Identifying the rise of multi drug resistant E. coli

Escherichia coli. Credit: Rocky Mountain Laboratories, NIAID, NIH

Antibiotic resistance in E. coli has been steadily increasing since the early 2000s despite attempts to control it, a new study suggests. In the biggest genomic survey of E. coli to date, that took more than 16 years in Norway, researchers have successfully tracked the spread of antibiotic resistant genes and have shown that these genes are being transferred between E. coli strains.

Researchers from the Wellcome Sanger Institute and University of Oslo have tracked multidrug resistance in Norway and compared this to a previous study from the UK. They found that resistant strains developed around the same time, but increased more rapidly in the UK population.

The results, published today in The Lancet Microbe show that tracking these resistant strains is important in the surveillance and control of drug resistant E. coli, which poses a significant issue in hospitals where it can cause severe infection and mortality. In addition, understanding how these genes are transferred between strains, and what has caused them to acquire drug resistance can help prevent the growth of antibiotic resistance strains.

The bacterium, Escherichia coli is a common cause of bloodstream infections world-wide*, which seem to be increasing over the last decade. E. coli is commonly found in the gut, where it does not cause harm, but if it gets into the bloodstream due to a weakened immune system it can cause severe and life threatening infections. As an added challenge for health care providers, multi-drug resistance (MDR) has become a frequent feature of such infections, and in a worrying number of cases the available treatment options are becoming limited.

In the largest study of its kind, and only the second systematic longitudinal genomic study of bacteremia E. coli, researchers from the Wellcome Sanger Institute and the University of Oslo processed a nation-wide catalogue of samples from more than 3,200 patients to track antibiotic resistance over 16 years. By harnessing the power of large-scale DNA sequencing, they tracked the emergence of drug resistance and compared this to a similar study conducted in the UK**.

The team found that MDR started to increase and show in more strains in the early 2000s due to antibiotic pressure, and now multiple MDR E. coli strains are present in Norway. However, MDR E. coli seems to be more widely present in the UK, despite similar policies in place around antibiotic use. The UK population however is considerably larger than Norway which could explain some of the differences. Further research is needed to allow for closer comparison and to identify the exact factors that cause rapid spread in some locations compared to others.

MDR is relatively rare in bacteria. However, this new study has identified that lineages that previously were not thought to have MDR have acquired drug-resistance genes, showing the increased ability of E. coli to share MDR genes that move horizontally between strains.

Professor Jukka Corander, co-author and Associate Faculty member at the Wellcome Sanger Institute, said: "The high number of samples from the Norwegian population and the level of genomic detail on the strains of bacteria enabled us to make much more far-reaching conclusions than were ever possible before. This study demonstrates the power arising from a systematic national surveillance of resistant organisms, which both collects and makes the data available for in-depth analyses. Without these in place, it would have been impossible to approach the central research questions formulated in the study and find answers to them."

The researchers hope to conduct similar research in the UK to build on previous studies and gain a full data set of 16 years in the UK in order to more closely track MDR resistant E. coli.

Dr. Rebecca Gladstone, lead author of the study and Bioinformatician at the University of Oslo, Norway, said: "Being able to estimate the expansion timelines of the MDR clones of E. coli and to identify multiple occasions of novel acquisition of resistance genes is particularly exciting as this is the first time that this has been possible. Understanding and tracking the movement of these drug resistance genes and the strains that carry them are necessary for controlling the spread of drug-resistant bacteria, which is a huge issue in healthcare."

Professor Julian Parkhill, co-author and Professor in the Department of Veterinary Medicine at University of Cambridge, said: "Long-term studies such as this one provide in-depth understanding about the complex epidemiology underlying bloodstream infections. The next step would be further research to detail the factors determining the success of emerging pathogenic clones of these bacteria, to help find a way to control and possibly minimise the spread of multidrug resistance."

*Kern WV, Rieg S. (2020) Burden of bacterial bloodstream infection - A brief update on epidemiology and significance of multidrug-resistant pathogens. Clin Microbiol Infect 26: 151-7.

**Teemu Kallonen et al. Systematic longitudinal survey of invasiveEscherichia coliin England demonstrates a stable population structure only transiently disturbed by the emergence of ST131, Genome Research (2017). DOI: 10.1101/gr.216606.116


ESCHERICHIA COLI

Escherichia coliis a facultative, enteric, Gram-negative, motile/flagellated, and lactose-fermenting rod that occur in the genus Escherichia and family Enterobacteria or Enterobacteriaceae. Enterobacteriaceae are bacteria that naturally exist in the intestinal tract of animals and humans, and also found in water and soil. Because the natural habitat of E. coli is the intestinal tract of humans (animals inclusive), it is therefore used as an indicator of the faecal contamination of drinking water and water used for other domestic, pharmaceutical and industrial purposes. As a baseline, 100 ml of drinking water must not contain any trace of E. coli.While most enteric Gram-negative bacteria such as Shigella and Salmonellaare important and regular human pathogens, E. coli are members of the normal intestinal flora and may only cause disease by chance. Basically, E. coli causes pathological conditions in humans when they become transient (i.e., when they leave their normal site in the intestinal tract of humans to tissues or parts of the body that are outside the intestines). It is noteworthy that all bacteria in the Enterobacteriaceae family are also called coliforms.

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A coliform is a Gram-negative non-sporulating facultative rod that ferments sugars (such as glucose and lactose) to produce gas within 48 h at 35 o C. The term coliform can also be used interchangeably with commensals. Though E. coli is a less common human pathogen, it is the most common cause of uncomplicated cystitis in man. Cystitis is a bacterial infection that occurs when faecal bacterial flora (e.g., E. coli) gains entry into the urethra and bladder of normal or healthy individuals. Pathogenic strains of E. coli are the commonest and leading causes of urinary tract infections (UTIs) in human population, and they have also been implicated in other diseases such as bacteraemia, diarrheal diseases and sepsis. For example, E. coli O157:H7 is an E. coli strain reserved in cattle/cow but causes haemorrhagic colitis. Haemorrhagic colitis is a zoonotic disease in man, and it is transmitted through the feacal-oral route. It is noteworthy that the alphabets ‘O’ stands for cell wall antigen while ‘H’ stands for flagella antigen as seen in E. coli O157:H7 strain. The capsular antigen of bacteria (e.g., Klebsiella species) is often represented with the alphabet “K”. E. coli is also amongst the top pathogens isolated from postsurgical wounds. In effect, E. coli is more of an opportunistic pathogen than a true pathogen, and its pathogenic strains are notorious in causing nosocomial (hospital-acquired) infections. E. coli is also implicated in a number of community-acquired infections and they are also responsible for a number of hospital visits in developing countries where personal and environmental hygiene, as well as access to potable water is still in a pitiable state. Biochemically, E. coli is indole positive, haemolytic on blood agar and they ferment sugars to produce gas.

PATHOGENESIS OF ESCHERICHIA COLI INFECTION

E. coli is the most common normal flora of the intestinal tract of humans, and they can also be found in the genital tract and upper respiratory tracts in traces. The presence of pathogenicity islands (acquired foreign DNA) in the genome of enteropathogenic E. coli enhances the pathogenicity and/or virulence of the organism. Infections resulting from E. coli occur occasionally and this has been attributable to the relocation of the bacteria from its normal location in the intestine to other extra-intestinal sites in the body. E. coli is implicated as causative agent in a number of infectious diseases including but not limited to UTI, diarrheal diseases, meningitis, wound infections and peritonitis. They produce various types of toxins including shiga toxin, labile toxin, and stable toxins. These toxins help to increase their virulence in the host cells. Though E. coli is implicated in a handful of human infections when they have the opportunity, diarrheal diseases and UTIs are amongst the two most important E. coli infections that characterize the majority of hospital visits across the world. Based on their virulence, there are basically five groups of E. coli­-associated diarrheal diseases.

Urinary tract infections caused by E. coli usually arise from the entry of uropathogens into the bladder. Uropathogens (e.g., E. coli)can gain entry into the human bladder through sexual intercourse or some minor strain experienced during sexual activity. Urinary tract infections (UTIs) are caused by the presence and growth of bacteria (e.g., E. coli)anywhere in the urinary tract system including the kidney, bladder and the urethra. Most cases of UTIs are asymptomatic but some are symptomatic and may present with some clinical signs and symptoms such as increased frequency of urination, dysuria and haematuria (i.e., blood in urine). UTIs affect either the upper urinary tract system (e.g., the kidney and ureter) or the lower urinary tract system (e.g., the bladder and the urethra) of both males and females. However, UTIs are common health-associated infections in women than in men due to the shortness of the female urethra (which is about 1.5 inches) compared to that of their male counterparts (which is about 8 inches). This natural anatomical difference in the urethra of males and females makes the contamination of the female’s urinary tract system from the external genitalia almost unavoidable.

The female urethra is particularly prone to bacterial infection or invasion following the migration of pathogenic microorganisms from the anus or vagina. Pregnancy is another predisposing factor that increases the risk of acquiring a UTI. In pregnancy, physiological changes in the urogenital tract of expectant mothers increase their potential for pathogenic colonization by microbes such as E. coli that may eventually result to a UTI. Thus pregnant women are at a very high risk of acquiring a UTI beginning from week 6 through week 24 of their pregnancy than non-pregnant women. The anatomical positioning of the uterus (womb) during pregnancy (which allows it to overlie the bladder and increase urine retention in the organ) coupled with possible poor hygiene and hormonal changes that occur during pregnancy makes it probable for a UTI to occur more in pregnant women than in non-expectant mothers. The use of anti-sperm agents such as spermicides also increases the risk for a UTI in women (pregnant ones inclusive). The ability of E. coli to produce a UTI is also associated with the virulence of the organism such as its ability to produce toxins and having appendages (e.g., pili and fimbria) and other virulence factors that allows it to attach firmly to epithelial surfaces in the body.

PATHOGENIC STRAINS OF ESCHERICHIA COLI THAT CAUSES DIARRHEAL DISEASES IN MAN

  • ENTEROPATHOGENIC E. COLI (EPEC): EPEC strains causes diarrhea in infants and children in developing countries. EPEC strains adhere strictly to the epithelial cells of the intestines by means of an adhesion molecule and start proliferating. They cause lesions known as effacing or attaching-effacing lesions that affects the microvilli of the intestines, and this lead to profuse and prolonged diarrhea in infants. Vomiting can also be accompanied in an EPEC strain infection. The diarrhea caused by EPEC strains is generally self-limiting but can be chronic and last longer in the infected children depending on their immune state. The mode of transmission of this type of E. coli­-associated diarrheal disease is via the feacal-oral route.
  • ENTEROTOXIGENIC E. COLI (ETEC): ETEC strains are the main causative agents of traveler’s diarrhea in people visiting developing countries. It causes watery diarrhea in both infants and adults. ETEC strains produce a variety of enterotoxins that are responsible for the watery diarrhea they produce in their host. The enterotoxins (which are heat-stable and heat-labile in nature) bind to the epithelial cells of the intestines where they stimulate guanylate cyclase that activates the production of cyclic guanosine monophosphate (cGMP). This action mediates the inhibition of sodium ions (Na + ) and stimulates the secretion of chloride ions (Cl – ) and/or electrolytes and water into the lumen of the small intestine that finally result into watery diarrhea. The mode of transmission of this type of E. coli­-associated diarrheal disease is via the feacal- oral route especially through the consumption of foods contaminated with human feaces.
  • ENTEROHAEMORRHAGIC E. COLI (EHEC): EHEC strains are the causative agents of haemorrhagic colitis (a life-threatening bloody diarrhea), and they mainly affect the colon (large intestine) unlike other pathogenic strains of E. coli that attack solely the small intestines. They cause severe abdominal pain followed by bloody diarrhea and haemolytic uraemic syndrome (HUS) in humans. EHEC strains produce verotoxins (a shiga-like toxin) and are sometimes called verocytotoxin-producing E. coli (VTEC) because their toxin is cytotoxic on Vero cells (that originated from kidney cells of African green monkeys) in tissue cultures. Consumption of food stuffs such as beef and other meat products from animals colonized by the bacteria are the main source of acquiring the pathogen. Spinach and unpasteurized fruit juices can also aid in the transmission of EHEC strains. EHEC disease (bloody diarrhea) is a disease of the developed countries. It occurs at a low frequency in developing countries. E. coli 0157:H7 serotype is a major form of EHEC strains as both are genetically related. The mode of transmission of this type of E. coli­-associated diarrheal disease is via the feacal-oral route.
  • ENTEROINVASIVE E. COLI (EIEC): EIEC strains cause E. coli-associated dysentery that resembles shigellosis. Shigellosis is caused by Shigella dysenteriae.Though EIEC infection may occur worldwide, children under the age of 5 years old and who live in developing countries are mostly affected by the disease.EIEC is toxigenic (i.e., it produces enterotoxins), and they penetrate the colonic mucosa and/or epithelial cells of the intestine where they cause inflammatory ulcerations that result in dysentery. The stool of infected patients is usually accompanied with blood, mucous, and pus cells. Contaminated food and water are the main source of acquiring the EIEC infections. The mode of transmission of this type of E. coli­-associated diarrheal disease is via the feacal-oral route.
  • ENTEROAGGREGATIVE E. COLI (EAEC): EAEC stains are the causative agents of food-borne disease in developed countries, as well as chronic and acute diarrhea in people living in developing countries. They cause vomiting and watery diarrhea in infants and children living in developing nations. EAEC strains are notorious in adhering tightly to the intestinal mucosa of its human host to form biofilms or aggregates of bacterial cells. This type of E. coli-associated diarrhea is often associated with neonatal-nurseryoutbreaks in hospital settings. The mode of transmission of this type of E. coli­-associated diarrheal disease is via the feacal-oral route.

LABORATORY DIAGNOSIS OF ESCHERICHIA COLI INFECTION

The laboratory diagnoses of E. coli-associated diarrheal diseases are mainly based on microscopy and isolation of the infecting pathogen from clinically important specimens. Blood, urine, stool, and pus are some of the specimens obtained for laboratory analysis. A mid-stream urine (MSU) is required to diagnose UTI caused by E. coli in the laboratory. Bacterial counts of E. coli less than 10 3 colony forming unit (CFU) per ml of urine indicate contamination while counts above 10 5 CFU/ml of urine are a strong indication of E. coli infection (i.e., significant bacteriuria). Bacteriuria is the presence of bacteria in urine. E. coli grow on MacConkey agar to produce smooth pink colonies (Figure 1), blood agar (to produce mucoid and haemolytic colonies for some strains), cystein lactose electrolyte deficient (CLED) medium (to produce yellow colonies) and on Hektoen enteric agar (to produce yellow colonies). It also grows on triple sugar iron agar (TSIA) or Kligler iron agar (KIA) where some strains of E. coli produce gas (hydrogen sulphide, H2S) and acid. Sorbitol MacConkey agar is specifically used to screen for E. coli O157:H7 strain. Biochemically, E. coli strains are lactose fermenters, indole positive, lysine decarboxylase (LDC) positive, and they reduce nitrate to nitrite in dipstick analysis of urine test. Molecular detection techniques for prompt identification of E. coli strains include the use of PCR and DNA probes.

Figure 1. Escherichia coli growing on MacConkey agar plate. E. coli is a lactose fermenter and it produces smooth pink colonies on MacConkey agar (arrows). Photo courtesy: https://www.microbiologyclass.com

IMMUNITY TO ESCHERICHIA COLI INFECTION

There is no long-lasting immunity associated with E. coli-associated infections even though some appreciable levels of specific and non-specific resistance may be mounted during the onset of the disease. However, there is low incidence of the disease in breast-fed infants, thus underscoring the protective function of the maternal antibody transferred via breast milk.

TREATMENT OF ESCHERICHIA COLI INFECTION

Most cases of gastroenteritis caused by bacteria in the Enterobacteriaceae family (E. coli in particular) are self-limiting and often heal without any antibacterial therapy. Since E. coli-associated diarrheal diseases are often accompanied with the loss of fluids and electrolytes from the body, treatment and management of the disease should be started with fluid and electrolyte replacement. Administration of oral-rehydration therapy (containing specific amount of salt, sugar and water) to counter the possible dehydration in the diarrhea patient is the best form of supportive therapy because it returns the affected individuals to a normal fluid and electrolyte state of the body. Though some strains of E. coli may be resistant to some antibiotics, sulphamethoxazole-trimethoprim, doxycycline, fluoroquinolones, cephalosporins and aminoglycosides still have remarkable antibacterial effect on the pathogen. But the physician’s choice of using any of these agents should be guided by the susceptibility test results for each patient’s E. coli in order to reduce the emergence of resistance, and thus guarantee appropriate treatment and prognosis.

PREVENTION AND CONTROL OF ESCHERICHIA COLI INFECTION

The presence of E. coli in drinking water and water meant for other domestic or industrial purposes is enough indication of faecal contamination of the water source from either sewage or human feaces (especially in places where people defecate in water bodies). Food meant for human consumption becomes contaminated with the pathogen when such water sources are used for either food processing or food preparation. Thus, the prevention of E. coli-associated diarrheal diseases involves avoiding the consumption of contaminated water and food. Travelers or tourists visiting tropical countries should ensure that they only eat properly cooked food and drink only bottled and well disinfected water. Uncertain fruits, vegetables and water should be avoided as much as possible. People working in hospital facilities, clinics and other medical establishments should imbibe strict or good personal hygiene such as hand washing since E. coli and other enteric bacteria are opportunistic pathogens that can easily be transmitted from one person to another or from one body part to another where they cause infection.

Further reading

Brooks G.F., Butel J.S and Morse S.A (2004). Medical Microbiology, 23 rd edition. McGraw Hill Publishers. USA.

Gilligan P.H, Shapiro D.S and Miller M.B (2014). Cases in Medical Microbiology and Infectious Diseases. Third edition. American Society of Microbiology Press, USA.

Madigan M.T., Martinko J.M., Dunlap P.V and Clark D.P (2009). Brock Biology of Microorganisms, 12 th edition. Pearson Benjamin Cummings Inc, USA.

Mahon C. R, Lehman D.C and Manuselis G (2011). Textbook of Diagnostic Microbiology. Fourth edition. Saunders Publishers, USA.

Patrick R. Murray, Ellen Jo Baron, James H. Jorgensen, Marie Louise Landry, Michael A. Pfaller (2007). Manual of Clinical Microbiology, 9th ed.: American Society for Microbiology.

Wilson B. A, Salyers A.A, Whitt D.D and Winkler M.E (2011). Bacterial Pathogenesis: A molecular Approach. Third edition. American Society of Microbiology Press, USA.

Woods GL and Washington JA (1995). The Clinician and the Microbiology Laboratory. Mandell GL, Bennett JE, Dolin R (eds): Principles and Practice of Infectious Diseases. 4th ed. Churchill Livingstone, New York.


How the E. coli Bacterium Can Benefit Us

The bacterium Escherichia coli is often thought of as a pathogen, but it&rsquos typically found in the intestine as a regular part of gut flora. New work by researchers at the University of Colorado Boulder has now shown that it&rsquos a vital part of that microbial community because it helps cells absorb iron, an essential nutrient. Reported in Cell, this study sheds light on how gut bacteria are beneficial to our health, and may also improve therapeutics that aim to treat iron deficiencies.

"In recent years, we have begun to realize that many microorganisms populating the human gastrointestinal tract are good for us, but we are only beginning to discover exactly what benefits they offer and how," said senior author Min Han, a professor in CU Boulder's Department of Molecular, Cellular and Developmental Biology (MCDB). "This new finding identifies one key role of E. coli, and that is to help cells absorb iron."

Iron deficiency is a very common problem, all over the world. It&rsquos a major cause of anemia, in which the body doesn&rsquot have enough blood cells. The disorder impacts more than one billion people worldwide.

There are pathogenic strains of E. coli that can cause big problems when they get out of the intestinal tract, for example, when it contaminates food that people consume. It is a common microbe, however, that isn&rsquot usually harmful. Han and research associate Bin Qi wanted to learn more about the potentially beneficial roles it plays.

It&rsquos been established that E. coli makes a chemical called enterobactin so it can absorb its own iron. But it had been assumed that in doing so, it was taking iron from its host. This work challenges that idea and suggests that enterobactin binds to ATP synthase, a molecule in host cells, drawing in iron.

For this study, the researchers used the roundworm, C. elegans, as a research model. The worm is a natural host for E. coli. The scientists also created E. coli that could not produce enterobactin and as a result, grew slowly and had low iron levels. After the worms were exposed to enterobactin, they resumed normal growth and their iron levels increased.

The scientists then found that when human cells or worms were given enterobactin, their iron levels went up even when iron was not also added.

"While bacteria make this iron-scavenging compound for their own use, our research suggests that mammals - including humans - have learned over time to hijack it for their own benefit," said Han, a Howard Hughes Medical Institute investigator.

While iron supplements can be helpful to some, Han noted that they may also suppress the production of enterobactin, and thereby interfere with iron uptake. Antibiotics could do the same thing, he added.

"Ultimately, we believe this molecule has great potential for addressing iron deficiency disorders, which are so prevalent," Han said. "Studies like ours demonstrate just how host animals are benefiting from the activities of the huge number of microbes in their gut."

Han is pursuing a patent for this work and intends to continue to develop therapeutics that can replace or improve iron supplementation.

Learn more about how the gut microbiome impacts human health in this recent lecture presented by the National Institutes of Health, featuring Fiona Powrie, the head of the Kennedy Institute of Rheumatology at the University of Oxford.


The main job of the urinary system is to eliminate waste, regulate electrolytes, and maintain water balance in the body.

This process starts with the kidneys that filter the blood and the production of urine. The urine travels through the ureters to reach the bladder, where it is stored.

When urinating, the bladder empties and the urine travels out of the body through the urethra. A urinary tract infection severely affects the kidneys, bladder, ureters, or urethra.

An infection usually occurs when the bacteria that live inside the intestine find their way into the urinary tract through the urethra.

What is this bacteria in the urine?

The Escherichia coli or E. coli , a bacteria normally found in the intestines of humans and animals. It is responsible for more than 85 percent of all urinary tract infections.

Not only is there one type of E. Coli, and there is a wide variety of infections and negative symptoms that can occur when this bacteria becomes a problem. But there are also some types of E. coli that are completely harmless.

Other common bacteria also cause urinary tract infections, including Staphylococcus Saprophyticus, Pseudomonas aeruginosa, Klebsiella and the pneumonia virus.

Have you ever had a painful urinary tract infection? They are quite hard to forget. Most likely, the bacterium Escherichia Coli caused that infection.

Surely you already know that bacteria, we often worry about it in regards to our food and our digestive systems.

What are the symptoms of E. coli infection in the urine?

What this bacterium does to your body depends to a large extent on the type of E. coli it has and what type of infection it is causing. It usually presents the following symptoms:

  • Urination (urination) that burns.
  • Frequent urination urges, even if there is almost no urine.
  • The urine is smelly, cloudy or bloody.
  • Fever or chills
  • Pelvic pain in women and rectal pain in men.
  • Pain in the lower back, abdomen, hips.
  • Bruises and pale skin.
  • Weakness.
  • Cold.

Urinary tract infections are not usually serious, but they can be dangerous if the bacteria make their way into the kidneys.

If left untreated, a kidney infection (considered a UTI – Urinary Tract Infection ) can cause permanent kidney damage and even deadly blood poisoning.

How can we get infected with this bacterium? – Causes

Since E. coli is transported in the stool, not washing your hands after defecating becomes a real problem for everyone around you. As it can get to your hands (invisible, of course), then it can reach everything else.

In the same way, coming into contact with animals (which obviously are not cleaned after the depositions) is an easy way to pick up the bacteria.

All this is reduced to washing hands, after using the bathroom, after touching animals or after being near crowds (especially schools).

Escherichia coli can sometimes be found in water. If an animal (or human) has gone to the bathroom near a water source, it can be found in drinking water.

Much of our exposure to E. Coli comes from food handling. Problems can arise when we do not properly clean the products, we eat food that was not stored at the right temperature, we do not cook the meat at the right temperature and we use utensils or dishes that have not been cleaned properly.

In conclusion we must handle the food with care, ensuring that the meat is well cooked, and take the time to wash the products and cooking surfaces.

How is this bacteria lodged in the urine?

People and animals usually have some E. coli in their intestines, but some strains cause infection.

The bacteria that cause the infection can enter our body in a large number of ways.

Inadequate handling of food.

If the food is prepared at home, in a restaurant or in a grocery store, mishandling and preparation can cause contamination.

The most common causes of food poisoning include:

  • Do not wash your hands completely before preparing or eating food.
  • The use of utensils, cutting boards, or serving food on dishes that are not clean, causing contamination.
  • Dairy consumption or food that has been left out too long.
  • Consumption of foods that have not been stored at the correct temperature.
  • Consumption of foods that are not cooked at high temperatures, especially meats and poultry.
  • Consumption of seafood without cooking.
  • Drink milk without pasteurizing.
  • Consumption of raw products that have not been washed correctly.

Connection E. Coli and urinary tract

E. Coli causes almost all urinary tract infections, about 85% of them. While other bacteria such as Staphylococcus can also cause these painful infections, it is important to understand why E. Coli is the “king of urinary tract infections”, so to speak.

Often we will have E. Coli in our own body. So in one way or another, E. Coli reaches our urethra.

This happens often (in the case of women) when they are cleaned from back to front. Although sexual intercourse is another common way of producing this spread in both sexes.

Also keep this in mind. Women have many more infections in the urinary tract than men, this is largely due to their urethras.

Not only is a female urethra considerably shorter (which shortens the trip E.Coli has to do to reach the bladder), but it is also very close to the anus.

As much as we do not want to think about it, that proximity leads to the contamination of bacteria.

Is there any treatment?

Treatment for an E. coli intestinal infection involves resting and drinking plenty of water to restore fluids lost through diarrhea and vomiting. Oral serum is recommended.

Drink as much water as you can because this will help dilute the urine and also relieve the burning sensation.

Antibiotics are not recommended, as they can triple the risk of developing hemolytic uremic syndrome (HUS), a condition in which Shiga toxin destroys red blood cells and platelets (which help the blood to clot), finally causing kidney failure.

Antidiarrheal medications may also increase the risk of developing hemolytic uremic syndrome, according to a 2011 article in the journal Clinical Infectious Diseases .

However, antibiotics and antispasmodic agents may be useful for other types of E. Coli, such as Enterotoxigenic E. Coli, which causes traveler’s diarrhea.

In the absence of severe symptoms, such as bloody diarrhea or severe abdominal pain, some doctors believe that the use of antidiarrheal medications is acceptable.

Do not drink drinks that can irritate your bladder. You should avoid alcohol, coffee and soft drinks that contain citrus juices.

Applying a heating pad directly on your abdomen will also relieve the pressure and discomfort of the bladder.

You may also consider using alternative medications to treat your urinary tract infection after you have found E. coli in the urine culture.

Drinking cranberry juice is one of the many things you can do to relieve pain. The juice has properties to fight infections. There are chances that cranberry juice will not work for you, but if it does, there is no secondary damage.

However, you should avoid taking cranberry juice if you are already taking anticoagulant medications such as aspirin.

Antibiotics are not recommended, as they can triple the risk of developing hemolytic uremic syndrome, a disease in which the Shiga toxin destroys red blood cells and platelets (which help blood clot), ultimately causing renal insufficiency.

However, when the infection is very severe, it is most viable to treat urinary tract infections with rounds of antibiotics.

Your doctor may prescribe antibiotics in low doses that you should take for six months or longer. You may be prescribed specific antibiotics to take after a sexual encounter, this is usually the case when your urinary infection is related to sexual activity.

A serious urinary tract infection usually requires hospitalization with treatment with intravenous antibiotics.

This can kill the bacteria (which, as we already know, is probably E. Coli). Ciprofloxacin (or Cipro for short) is a common option.

Although certain types of E. coli can be quite severe, urinary tract infections are generally quite harmless, although annoying and painful.

What happens there is resistance to antibiotics?

As time goes by, more and more E. coli bacteria become resistant to antibiotics.

In fact, between 2000 and 2010, scientists discovered that the amount of E. coli resistance to common antibiotics (such as Cipro) “increased substantially.”

This is a real problem. If antibiotics do not work, we may have a real problem when an infection becomes severe.

Why is it happening?

First, antibiotics are being widely prescribed. About 80% of people who come to the doctor with sinus problems will receive a round of antibiotics, although it is entirely possible that it is a virus and not a bacterial infection.

We are also increasing our exposure to the foods we eat. Antibiotics are also prescribed strongly to animals (often in the foods they eat). Then we eat those animals.

One study showed that the prevalence of E. coli resistant to antibiotics in broilers is quite high.

So what else can we do with E. coli bacteria and urinary tract infections?

Is there any hope for treating urinary tract infections when antibiotics are less and less effective?

Absolutely! Here are some natural health boosters that have been scientifically proven to help urinary tract infections:

Take a D-mannose supplement: this natural sugar was observed in a study of more than 300 women. Some received D-mannose, other antibiotics and others no treatment.

In six months, the D-mannose group only had a recurrent urinary infection rate of 14.6% the group of antibiotics had 20.4%. In addition, the D-mannose group showed fewer side effects.

Try a hibiscus extract supplement: several studies have shown that hibiscus extract is an effective inhibitor of E. Coli.

Prevent spreading: do proactive things to prevent the spread of E. Coli to the urinary tract. This includes cleaning from front to back, washing your hands frequently and using the bathroom immediately after intercourse.

Of course, you should also drink plenty of water, take a probiotic (good bacteria are important here) and make sure your diet is full of foods that improve the immune system.


Bacteria- E coli, K-12 strain, live broth

Description: B1 is a 10 mL vial of E coli Bacteria (K-12 strain) live broth. E. coli is a common gram-negative rod-shaped bacterium, found in normal human (and other animals) bacterial flora. Most E. coli strains are harmless but some strains can cause severe and life-threatening diarrhoea. The harmless strains are part of the normal flora of the gut and can benefit their hosts by producing vitamin K2 and by preventing the establishment of pathogenic bacteria within the intestine. E. coli 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 faecal contamination.

Qty: 1 10 mL vial of Broth

Optimal growth of E. coli occurs at 37°C but some laboratory strains can multiply at temperatures of up to 49°C.


Escherichia coli

Escherichia coli (or E. coli for short) is a bacterium that occurs naturally in the intestines of people and animals. There it provides protection against harmful bacteria. However, some strains can cause food-borne infections.

Escherichia coli (or E. coli for short) is a bacterium that occurs naturally in the intestines of people and animals. There it provides protection against harmful bacteria. However, some strains can cause food-borne infections.

Escherichia coli occurs naturally in the intestines of people and animals. Even though E. coli has a bad name, this bacterium is still very useful to us. In the large intestine, it prevents the uncontrolled growth of harmful bacteria.

Beneficial intestinal bacterium

E. coli is the most well-known intestinal bacterium. In popular terms, E. coli is even known as the ‘poo bacterium’. This is remarkable, as there really aren’t so many of them in your intestines. The reason that it is so well known is mainly due to its role in microbiology. It is used, for example, in the testing of drinking water. Unlike many other gut microbes, E. coli can also survive for a long time outside the body. It is found in places such as water taps, door handles or in water. Therefore, this bacterium is widely used to reveal possible traces of poo in drinking water.

Pathogen

E. coli is generally important for intestinal health. This bacterium occurs in a variety of strains, most of which do not cause disease symptoms. However, some strains can be dangerous. They can occur in raw meat, raw vegetables and unpasteurised milk products.

E. coli as a model species

A harmless type of E. coli has been used in various types of research since 1927. One advantage of E. coli is that it divides rapidly. As a result, scientists can culture many generations in a short period of time. Furthermore, its genome is composed of relatively simple genes, and has been fully mapped. All of which makes this bacterium highly suitable for the purposes of science.


Watch the video: Pathogenic strains of E. coli and their molecular mechanisms (September 2022).


Comments:

  1. Nabil

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  2. Stillman

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  4. Carmelo

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  5. Kazrashakar

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  6. Barrak

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  7. Jordon

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