Escherichia Coli: characteristics, pathogenicity and prevention

Escherichia coli bacterium was initially isolated and described by the German pediatrician Escherich in 1885, who proved its existence as a regular host in the intestine. He named it Bacterium coli commune, which can be translated as „common colon bacteria“.

In 1919 Castellani and Chalmers gave it its definitive name in homage to Escherich. Escherichia quickly became the genus typical of the Enterobacteriaceae family and E. coli in the best-known species of this genus.

Theodor Escherich (Ansbach, 1857 – Vienna, 1911) German bacteriologist.

Escherichia coli characteristics

E. coli have Gram negative, non-sporulating bacilli, produce indole from tryptophan, do not use citrate as a carbon source and do not produce acetoin. In addition, they ferment glucose and lactose with gas production.

Like all Gram-bacteria, the E. coli envelope consists of three layers: the cytoplasmic membrane, the outer membrane and, between both, a periplasmic space made of peptide-glucan. This structure gives the bacteria its shape and rigidity and allows it to withstand relatively high environmental osmotic pressures.

E. coli are mesophilic bacteria that develop optimally around warm-blooded animals body temperatures (35-43 ºC). The growth limit temperature is approximately 7ºC, which indicates that an effective control of the cold chain in food industries is essential to prevent E. coli growth in food. Freezing has little effect on E. coli population in food and does not guarantee the destruction of a sufficient number of viable bacteria to ensure its safety. However, E. coli is sensitive to temperatures above 70°C. At higher temperatures they are easily eliminated. This is why pasteurisation of food like milk, juices, etc., is very important in order to guarantee their elimination.

Besides temperature, pH and water activity can influence the proliferation of E. coli. The optimal development conditions for these parameters are 7.2 and 0.99 respectively. E. coli development stops at extreme pH (below 3.8, or above 9.5), and aw values below 0.94. Thus, the acidity degree of a food can be a protection factor and ensure its safety.

E. coli has multiple characteristics and aspects, and it is the best studied bacterial taxon, although knowledge regarding wild strains is still incomplete. It seems that the adapting ability of these bacteria is rare, due to the acquisition of new genotypes from plasmids, bacteriophages, and other elements that transmit their genetic material. Moreover, its known capacity for ubiquity promotes the repeated appearance of strains with new properties, including pathogenic abilities not easily recognisable.

Adhesion mechanism

Serotype characterisation is the first technique that enabled differentiating commensal from pathogenic strains, it is done by studying the virulence properties that are directly linked to E. coli pathogenic capacity. Several factors that intervene in the E. coli pathogenic power have been described, among which are the adhesion factors. Adhesion is determined by the presence of fimbriae, which give cells the ability to specifically bind to a cellular receptor. Fimbriae are fine filaments of a protein nature arranged around the bacteria and with a termination that adheres to the cellular receptor. This adhesion is performed by an outer membrane protein called intimin, which plays an essential role in anchoring E. coli onto epithelial cells of mammals, favouring the first colonisation stage.

The bacteria firstly adhere to a white intestinal cell by binding and fitting into its receptor, called the intimin translocator receptor (Tir), located on the host’s epithelial cell membrane. The bacteria attach to intestinal cells by binding their intimin proteins to inserted Tir proteins. It has been noticed that the protein complex has rigid extensions with securing structures located at the end of the intimin, which are stretched to grasp the receptor. The protein arms are bent in such a way that they are able to hold the bacteria against the surface of the intestinal cell. The crystallographic structure demonstrates that each Tir consists of two units, which form a structure called dimer. The dimerisation intertwines the system, like the surfaces of a closure that stick together. When there is only one single pair of intertwined points, the closure strength is weak, but if there is a whole group of them, a good adhesion is achieved. By joining the intestinal cell, the bacteria probably use endless unions between intimin and Tir, and since E. coli are large bacteria, when there are many of these complexes binding them to the surface, a strong adhesion is achieved, given the resistance of these elements.

E. coli pathogenicity

Several E. coli strains can be found in human pathology with a marked virulence. They are known as agents responsible for childhood gastroenteritis, especially in developing countries, causing the death of almost one million children every year due to dehydration and other complications. This family of pathogens also includes E. coli O157:H7, which in the USA causes at least 20,000 cases of bloody diarrhoea and more than 200 deaths per year, due to kidney failure that especially affects young children and the elderly.

The main intestinal pathogens, which are described according to the clinical symptoms they generate, and the pathogenicity factors expressed are: enterotoxigenic E. coli (ETEC), enteropathogenic E. coli (EPEC), enteroagregative E. coli (EAggEC), enterohemorrhagic E. coli (EHEC) and enteroinvasive E. coli (EIEC).

Pathogenicity factors

Pathogenicity is a function of some surface antigens and the toxins they generate. Thereby, fimbriae act by providing their adhesion capacity, O and K antigens have antiphagocytic and inhibitory properties of serum bactericidal substances, and are responsible for the virulence of invasive strains, whose synthesis is encoded by genes found in high-molecular weight plasmids. They have an endotoxin linked to lipopolysaccharide, especially lipid A, responsible for the pyrogenic action and, presumably, the vascular alterations that occur in generalised infections. Some strains can produce exotoxins responsible for diarrhoea, whose synthesis is encoded by the presence of plasmids (Ent plasmids), which in turn can contain genes associated with the adherence ability and other properties (production of colicins, haemolysins and resistances to antibiotics). A thermolabile (TL) and antigenic enterotoxin similar to the Vibrio cholerae enterotoxin is known to exist and act by activating adenyl cyclase, which in turn transforms ATP into cyclic AMP, producing an increase in water and electrolytes secretion. There may also be a low-molecular weight and non-antigenic thermostable (TS) toxin, which produces fluid accumulation in the intestine by a different and hardly known mechanism, probably by the guanylyl cyclase route. These toxins do not produce toxic or anatomical alterations in the enterocyte, but they do cause functional alterations (cytotonic enterotoxins), which is a characteristic of the enterotoxigenic E. coli. On the other hand, enteroinvasive E. coli strains are known for their ability to penetrate and invade intestinal epithelial cells. It is believed that their penetration capability is due to the presence of surface antigens, especially of outer membrane proteins, whose synthesis is encoded by plasmids, as shown in the Shigella genus.

Pathogenic strains

The possibility of producing enterotoxins similar to those produced by Shigella dysenteriae (cytotoxic enterotoxins) has been suggested in some E. coli enteropathogens (0:26) and they have a direct toxic action on the intestinal epithelium cells, responsible for destroying enterocyte microvilli and causing diarrhoea. It has also been shown that serotype 0:157 produces a cytotoxic enterotoxin (verotoxin) on the endothelial cells of the vessels responsible for haemorrhagic diarrhoea.

EHEC are a group of pathogenic bacteria responsible for several constantly increasing infections. In the 1980s, EHECS, and particularly serotype 0157:H7, were emerging pathogens. In particular, its importance for public health appeared in 1982, after an outbreak in the United States. These bacteria also caused various deaths in recent years (in Japan, the United States, Canada, Scotland and France). 100 different EHECs have been currently reported as Shiga toxin producers. EHECs are responsible for varied clinical manifestations, ranging from an ordinary diarrhoea to a haemorrhagic colitis that can evolve in 10% of the cases to a haemolytic and uremic syndrome (HUS) in children and elderly, or thrombotic thrombocytopenic purpura in adults, a blood disorder that causes the formation of blood clots in small blood vessels. This leads to a low platelet count (thrombocytopenia). There are also other non O157 E. coli and Shiga toxin producers (STEC) such as O55, O111, O26, O103:H2; O148:H8.

Similar Stories