Escherichia coli , also called colon bacillus or E.  coli. , is a Bactérie Intestin ale of the Mammifère S very common at the human being. Discovered in 1885 by Theodore Escherich, in saddles of Infant S, it is generally a fecal Coliforme Commensal. However, some Souche S of E. coli can be Pathogène S.

Description

E. coli is a bacillus negative Gram of the family of the Entérobactérie S. It is a common host of the intestinal microflora commensale of the Man and warm-blooded animals (mammalian and birds). Its establishment in the digestive tract is carried out during the first hours or days which follow the Accouchement. E. coli then constitutes throughout the life of the host the dominant bacterial species of the optional anaerobic microflora of the intestine. E. coli is undoubtedly the living organism more studied to date: indeed, the seniority of its discovery and its easy culture (cellular Division every 20 minutes with 37 °C in a rich medium) make of it a tool of study of choice. The profusion of scientific publications which mention it testifies some, and she plays the part of “plow horse” in all the laboratories of molecular biology.

History

Theodore Escherich, by observing the frequency of the diarrheas néonatales, had already raised the question of the implication of the colon bacillus in the entérites. After the Second world war, knowledge converged to establish the concept of virulence of certain stocks of E. coli . In the Years 1950, many stocks of E. coli were accused as an agent etiologic of infantile diarrheas. One knows now that certain “specialized” stocks of E. coli are associated with very diverse pathologies (including extra-intestinal), as well at the Man as in the animal; Diarrhea S, Gastro-enteritis S, infections of the urinary tract, Meningitis S, Septicaemia S, “Disease of the hamburgers”, the haemolytic and uremic Syndrome etc

In prevention, a monitoring of the SHU takes place at the National Reference Center of the E. coli, located in the unit of Biodiversity of the Emergent Pathogenic Bacteria at the Institute Pasteur (France), which is charged to study the pathogenic stocks.

Since the Years 1950, the bacteriologists tested, thanks to the antigenic differences of E. coli , to subdivide the species in Sérotype S by immunizing rabbits with antigens Somatique S and flagellar. The Sérogroupage remains the method currently most used.

The sérotype is the combination of the 2 antigens, somatic O and flagellar H, (examples: O157: H7 and O111: H8), whereas the Sérogroupe is given only by the antigen O (example: O157, O111). However the sérotype is not sufficient to characterize the E. coli pathogenic. Each sérotype is not necessarily correlated with the pathogenicity.

Life cycle

E. Stewart and Al PLoS Biology February 2005

Antigens and sérogroupage

The somatic antigen O, defining the sérogroupe, is contained in the lipopolysaccharides present on the bacterial wall of the stocks at gram negative. The flagellar antigen H is of proteinic nature entering the structure of whips (lash péritriche) allowing the mobility of the bacterium. The antigen K of surface is not always present but if it is present, it blocks the agglutinability of the antigen O.

Somatic antigens O

There are some more than 150. The somatic antigens are composed of lipopolysaccharides complex. Currently certain medical analysis laboratories use agglutination with serums to determine the sérogroupe, but this technique is limited by the increasingly high number of serums to manufacture, by the presence of agglutinations crossed between the antigens O of E. coli, Shigella and those of Salmonella, and by the passage of the creamy consistency of the colony to a rough consistency having for consequence the absence of synthesis of the antigen O. For this reason a molecular technique of sérotypage was developed. The antigen O belongs to the lipopolysaccharide (LPS) of the external membrane of the bacteria with gram negative. It contains a great number of repeated units of oligosaccharides from 3 to 6 sugars whose combination determines the diversity of the antigens O. the genes coding the enzymes implied in the synthesis of the antigen O are gathered in the cluster genes rfb. This cluster rfb can be amplified specifically thanks to a system of starters then, after restriction by the endonucléase MboII, a profile noted “R” can be obtained by electrophoresis, corresponding to a sérogroupe of E. coli (Coimbra and Al , 2000). A profile of electrophoresis is function of the site of the sites of restriction suitable for MboII. Thus all the gene clusters corresponding to a somatic antigen will have a profile of restriction which is clean for him. This profile R will be then analyzed with the Taxotron® software then compared with a database, under development perpetual. For example, the profile R will have a R111 number, corresponding to the sérogroupe O111obtenu with the serum.

Flagellar antigens H

The antigens H are not used for the identification of the E. coli pathogenic but are of great interest to the epidemiologic point of view: the identity of the antigen H constitutes an element to ensure that it is about the same stock.

The diversity of the antigens H is due to the various types of flagelline composing the structure of whips. It is whips it which allows bacterial mobility. Typing is also carried out by sero-agglutination, but is developed only in very rare laboratories in the world. However, certain stocks lose their mobility and are classified like nonmobile (Nm or H). A molecular technique of sérotypage thus was also developed to determine the antigen H. The antigen H is coded by the gene cop. The final parts NR and C of the flagelline are very preserved and it is the median part, more variable, which gives the specificity of the antigen H. the E. coli motionless also has the gene cop but is unable to synthesize one whips functional. After amplification and restriction of the gene cop, it is possible to typify the antigen H by comparing the profile obtained with a database of profile-type (Machado et al., 1998). For example, the profile cop (noted F) will have a F8 number, corresponding to the H8 type obtained with the serum.

Antigens of surface or envelope K

There exist 3 types of antigen K indicated by the letters L, have or B.

• the Ag L is most frequent but is thermolabile (it is destroyed in ½ h. with 100°C). Thus the heating causes a loss of the antigenic capacity, capacity to fix the agglutinins and capacity to mask Ag O.
• the Ag has is rare; it is Ag capsulaire (the E. coli encapsulated are relatively frequent in the urinary infections). Ag has is very thermostable (one needs a pressure-sealing to destroy it)
• the Ag B is always present at the E. coli entheropathogenes of GEI (infantile gastro-enteritis). It has an intermediate thermolability: after ½ h. with 100°C, it always remains of Ag B but Ag O can come into contact with the serum by " trouage" envelope, the fixing of the agglutinin is always positive but the antigenic capacity is lost gradually (according to the duration of heating).

Difference between Ag B and Ag has or L : in a homogeneous population on limps from Petri,

• 80% of colonies + and 20% of colonies - for has or L
• distribution homogeneous in all the population for B

Identifying information of E. coli (step)

It is a bacterium of the family of the Enterobacteriaceae not having a Désaminase, which excludes the kinds Proteus , Morganella and Providencia (typically ex-tribe of the Proteae ).

It ferments glucose by the way of the mixed acids (Red of methyl +, VP -) what excludes the kinds Klebsiella , Enterobacter , Hafnia and Serratia (typically group of the KEHS, ex-tribe of the Klebsielleae ).

Moreover,

• Fermentation of the Lactose, Mannitol;
• Production of Indol starting from the Tryptophan;
• does not have a Uréase;
• does not produce a H₂S;
• Unable to assimilate the Citrate in Aerobiosis.
• ONPG+
• TDA-
• Urease
• Indol +++
• VP-

Genome

The genetic inheritance of the stock E coli of laboratory nonpathogenic was entirely sequence in 1997. Its genome includes/understands 4,6 million pairs of bases coding approximately 4200 proteins.

In 2001, the genome of a enterohemorragic stock of E coli (causing the disease of hamburger) was sequence. It includes/understands 5,5 million pairs of bases coding 5400 proteins. The following year, the genome of a stock of E coli causing urinary infections (cystitis, pylonéphrite) and meningitides néonatales, was sequence. It includes/understands 5,2 million pairs of bases coding 5300 proteins.

The comparison of the genomes of these three stocks of E coli reveals that only 40% their genes are common - as comparison, 99% of genes of the Man and of the large monkeys are common. This testifies to the remarkable evolutionary potential and the fickleness of this taxon bacterial. Indeed, the stocks of E coli pathogenic acquired during the evolution a gene repertory of virulence, which enables them to colonize new ecological niches by circumventing the mechanisms of defense of the host. The expression of a specific repertory of factors of virulence is correlated with a particular pathology and makes it possible to define different pathovars (see will infra ).

Plasticity of the genome of E. coli and pathogenicity

The concept of the bacterial pathogenicity resulting from a process multi-factor, implying a gene myriad, whose expression is chorégraphiée by processes of regulation is now well accepted. The expression of these genes allows a more effective adhesion, or the invasion of fabrics of the host, and thus allows the colonization of inaccessible or inhospitable niches for the E. coli commensaux . In this direction, the pathogenicity can be regarded as a selective advantage, and the success of a stock of E. coli as pathogenic probably requires the acquisition and the selection of genes of virulence, towards nonspecific recombinations and genetic transfers. The plasticity of the genome of E. coli is at the base of this process. The complete sequence of the genome of several stocks of E. coli watch the presence of many sequences of insertion (IS), bacteriophagic sequences, as of other beaches of unusual sequences which testify to the extraordinary plasticity of the genome of this bacterial kind. In fact the clinical isolates of E. coli have the largest genomes, whereas that of the E. coli of laboratory, nonpathogenic, makes 4,63 Mb. It appears thus that the ditch which separates the E. coli commensales from the E. coli pathogenic is with the acquisition of gene repertories of virulence. It could be that the acquisition of these genes is facilitated by an important aptitude to transfer. Indeed, more than 1% of the isolates of E. coli or Salmonella implied in food infections is “mutateurs” which presents a strong tendency to transfer, a phenomenon correlated with a deficiency in certain systems of repair of the DNA. The genes of virulence are generally localized on transmissible genetic elements as of transpose, the plasmides or the bacteriophages. Moreover, they can be gathered on large blocks of chromosomal DNA called “small islands of virulence”.

Escherichia coli , a bacterium commensale and an disease-causing agent

Certain specialized stocks of E. coli are associated with very diverse pathologies as well at the human being as at the Animal; diarrheas, gastro-enteritises, infections of the urinary Tract, meningitides, septicaemias, etc modern technologies of biochemistry, the genetics, molecular biology and cellular microbiology made it possible to identify and analyze the mechanisms implied in the interaction of the E. coli pathogenic with their host. It is interesting to note that in spite of the diversity of the affections caused by the stocks of E. coli pathogenic, all these stocks use a traditional strategy of infection, commune to many other disease-causing agents.

Like the majority of pathogenic of the mucous membranes, the stocks of E. coli responsible for diarrheas and infections extra-intestinal use a strategy of infection whose key points are the following: colonization of the mucous membranes, possibly invasion of the cells, multiplication, escape from defenses of the host, damage to the host.

To survive and multiply in the intestinal tract, the colon bacilli must surmount the first lines of defense of the organization host, namely the peristalsis and the effect of barrier of the microflora commensale. This microflora monopolizes the nutrients, product of the inhibiters and occupies surfaces of the mucous membranes. The effect of barrier is overcome by the E. coli pathogenic thanks to mechanisms which are known in general terms: the competition for the sources of carbon, iron, energy under anaerobic conditions, the production of bactériocines, as well as a strong growth rate. The stage of colonization implies also the capacity to be adhered to the surface of the intestinal mucous membrane. Virtually all the stocks of pathogenic enterobacteries or not have systems of adhesion, and it is well established that this capacity of adhesion is the characteristic most preserved at the E. coli pathogenic. The bacterial structures responsible for adhesion to the epithelial cells are adhésines fimbriaires (fimbriae or pili) or afimbriaires. Exposed to the surface of the bacteria, these adhésines interacts with receivers of the membrane of the target cells. Thus stocks of E. coli pathogenic are able partly thanks to their adhésines to colonize biotopes which or are not normally little colonized by the E. coli commensales. For example, the E. coli responsible for urinary infections deploy pili “P” (pili associated with pyelonephritides) which recognize glycolipides on the surface of the epithelial cells of the urinary tract.

The multiplication is essential in the process of pathogenicity; one conceives indeed that a fast multiplication is an advantage for colonization, as to cause damage before the immune system does not return in action. A slow multiplication, even its stop, can also constitute an advantage in the persistence of pathogenic which causes chronic diseases.

Another essential point in the process of pathogenicity is the interference of the E. coli pathogenic with the immune system of the host. It is known for example that certain types of lipo-polysaccharides (LPS; antigen “O”) presented to the surface of the bacteria protect them from the lytic action of the complement, of the fixing of the antibodies and phagocytosis. The polysaccharidic capsules (antigens “K”) which are secreted on the surface of certain stocks of E. coli pathogenic (mainly those causing of the extra-intestinal affections) can take part in the escape from defenses of the host. The capsules K1 and K5, which comprise homologies with molecules eucaryotes (the adhésines N-CAMWOOD and héparanes), have a low immunogenicity thus. The antigenic variations of certain proteinic molecules of surface (like the pili), can also take part in the avoidance of immunizing defenses.

The first stage of colonization carried out, certain pathogenic stocks produce powerful toxins, these last being able to be responsible alone for the damage inflicted with the host. Other pathogenic stocks divert with their advantage of the essential cellular functions, in order to survive and persist. Thus, by deteriorating the cellular cytosquelette, they can very strongly adhere to cellular surface (one speaks about adhesion “intimates”), even penetrate in the cells of the mucous membranes and multiply there, such Shigella flexneri or Salmonella typhimurium .

On the basis of these mode of interaction and clinical signs of the infection, the stocks of E. coli inductive of diarrheas can be currently classified into five pathovars: E. coli enterotoxigenic (ETEC), E. coli entéroinvasives (EIEC), E. coli enteropathogenes (EPEC), E. coli enterohemorragic (EHEC) and E. coli entéroaggrégatives (EAggEC). In addition to the E. coli inducing diarrheas, one distinguishes also the pathovar from the E. coli pathogenic extraintestinales (ExPEC) implied in not-intestinal affections: urinary infections, meningitides, septicaemias, mammites…

The E. coli enterotoxigenic (ETEC)

The ETEC are a major cause of acute aqueous diarrhea with dehydration in the children of low age (less than 3 years) in the countries in the process of development, and are also responsible for the “diarrhea of the travellers” (or “turista”). ETEC are also a frequent cause of often fatal diarrheas néonatales in livestock (calf, sheep, piglet).

The ETEC colonize primarily the part proximale small intestine, thanks to their “factors of colonization” (CFAx and CSx) which are adhésines fimbriaires. The ETEC do not induce marked histological deteriorations of the mucous membrane. The pathogenic capacity of the ETEC is explained mainly by the secretion of thermostable toxins (ST) and/or thermolabile (LT). Toxin LT, after endocytose, ADP-ribosyle the sub-unit alpha of the heterotrimeric protein Gs. It follows the hyper-activation of the adénylate cyclase, the increase in the concentration of the second AMPc messenger, and the phosphorylation of membrane conveyers - particularly the “CFTR”, the regulator of the membrane conductance implied in the mucoviscidose. This action results in a secretion of ion chloride and an inhibition of the absorption of sodium chloride by the intestinal cells, which causes the osmotic water diffusion towards the intestinal light. The action of the toxins ST is less known. While being fixed at their receiver on the surface of the intestinal cells (a guanylate cyclase), they induce concentrations increased in GMPc, which also results in activation from the CFTR, the deterioration of intestinal homeostasis, and an osmotic diarrhea. Thus, it is the action of the toxins ST and LT which explains the clinical picture of the infection: not very feverish aqueous diarrhea, abdominal nauseas and cramps.

The E. coli entéroinvasives (EIEC)

The EIEC are responsible for syndromes dysenteric characterized by an high fever, cramps abdominal and nauseas, accompanied by an aqueous diarrhea which evolves/moves quickly in a dysentery (saddles containing of blood and mucus). The EIEC are biochemical, antigenic, genetic and functional very close to those of the Shigella , and implement a similar mechanism of pathogenicity. The EIEC and the Shigella invade the intestinal mucous membrane on the level of the colonist, multiply, cause there cellular death and starting an intense inflammatory reaction. The process of invasion is complex and multi-factor, under the chromosomal dependence of loci and of a plasmide of virulence (pInv; ~220 KB). With regard to Shigella, the process of invasion can be summarized as follows: at the time of the contact with the epithelial cells, the bacteria secrete “invasines” (Ipa), which interact with cellular surface and cause a rearrangement localized of the cytosquelette leading to the penetration of the bacterium in the cell. Once in intracellular position, the membrane of the vacuole is quickly lysed thanks to a hemolysin of contact, releasing the bacteria in the cytoplasm where they can multiply. Then, the bacteria induce the polymerization of the cellular actine to one of their pole (thanks to IcsA) to be driven and be disseminated cells in cells. The process of invasion concerned by the EIEC remains to be been elucidated, but the current data indicate that it is probably identical to that of Shigella . The EIEC and the Shigella also work out one or more entérotoxines which would be implied in the episode of aqueous diarrhea which precedes the dysentery.

The E.coli enteropathogenes (EPEC)

the EPEC are responsible for infantile gastro-enteritises . It is generally admitted that these colon bacilli are pathogenic only below age the 2 years. Principal the sérotypes implied is O111 B4 and O119 B14… Most frequent in the EU these last years is O111 B4 but one starts to speak about other types. In the adult, in theory, the E. coli of GEI are not pathogenic. Some advance that certain diarrheas of the traveller would be due to types of E. coli particular unknown in the area where the traveller saw.

It is only in the infants in low-age that the disease takes a serious and epidemic form (especially and almost only in hospital medium). They are diarrheas with imbalance of the ionic balance; from where most important is to restore the ionic balance; the antibiothérapie will intervene secondarily.

The enterohemorragic E.coli (EHEC)

The EHEC are responsible for hemorrhagic colites. The principal tank of these bacteria is the digestive tract of the bovines; the human contamination is done via food, mainly beef chopped and believed milk. The sérotype O157 is most frequent. It is responsible for epidemics. The EHEC produce a verotoxine (or Shiga-toxin) which can involve a haemolytic and uremic syndrome (SHU). Epidemics with EHEC were declared following the contaminated and insufficiently cooked meat ingestion (hamburger). An epidemic took place in France in 2005. Cytotoxins (verotoxines) are at the origin of the destruction of the intestinal cells. The symptoms can go from the simple diarrhea to a bloody and abundant diarrhea. The demonstrations are more serious in the children of less than 8 years and at the people of more than 65 years. The haemolytic and uremic syndrome (SHU) appears amongst other things by a haemolytic anemia, a thrombopénie and an acute impaired renal function.

The entéroaggrégatives E.coli (EAggEC)

Until the beginning of the year 1980, the stocks of E. coli inductive of diarrheas were classified in three categories; ETEC, EIEC and EPEC, these last being then characterized primarily by their membership of distinctive sérotypes. With the beginning of the year 1980, it was noted that the majority of the stocks classified in the EPEC adhere on cells of line. Thereafter, three modes distinct from adhesion to the cells were described: “located” adhesion, “diffuse” adhesion, and “aggregative” adhesion, which made it possible to differentiate new a pathovar from E. coli diarrhegenic, EAggEC. EAggEC are currently defined as stocks which do not secrete the entérotoxines LT or ST, and which adheres to the cells culture by forming images “of brick cluster” (aggregative adhesion). It is probable that this definition includes nonpathogenic stocks; the heterogeneity of this group was confirmed besides by epidemiological studies and experimental infections of voluntary adults. Nevertheless, EAggEC are recognized more and more as being responsible for delays of growth and persistent diarrheas in the countries in the process of development like in the industrialized countries. Fimbriae (AAF/I and AAF/II) responsible for aggregative adhesion were described, but they are present in a minority of isolates of EAggEC. This suggests that the colonization of the digestive tract would be due to one or more fimbriae, like in the case of the ETEC. EAggEC adhere on the intestinal mucous membrane, enchased in a mucus biofilm produced by the cells out of goblets of the mucous membrane. Approximately 40% of the stocks of EAggEC produce the entérotoxine EAST1 (for “EAggEC St-like toxin”), which presents approximately 50% of homology with the toxin ST of the ETEC. The contribution of this toxin to the pathogenic capacity is not established yet. Also let us note that the gene coding toxin EAST1 or its variable was found in stocks EPEC and ETEC, like in stocks of E. coli pathogenic or not, which do not have the genes markers of the traditional pathovars.

The pathogenic E.coli extraintestinales (ExPEC)

(articles in the course of writing, patience!) PATIENCE EAST Of GOLD

Predator

Escherichia coli being a bacterium, it is sensitive to the Bactériophage S like the phages T4 and lambda.

See too

Pyelonephritis

Bibliographical sources of reference

Kaper JB and Al (2004) Pathogenic Escherichia coli. Nat Rev Microbiol 2:123.

External bonds

• Jtap '' and Al '' (2004) molecular Characterization of Escherichia coli of the sérogroupe O111. Institute Pasteur
• Model of '' E.coli '', statistics

Simple: Escherichia coli

Random links:

X-files, at the borders of reality | Gaston III of Foix-Béarn | Siniperca | The Intoxication of the capacity | Gerard Deprez