Category: Illness or disabilities
Introduction and description
Escherichia coli (commonly abbreviated E. coli) is a gram-negative, rod-shaped bacterium that is commonly found in the lower intestine of warm-blooded organisms (endotherms). There are a number of strains of this bacteria, as such one should look on it as a very large family of bacteria rather than a single pathogen.
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.
Most E. coli strains are harmless, but some serotypes are pathogenic. Each year, Enterotoxigenic E. coli [ETEC] , for example, causes more than 200 million cases of diarrhoea and 380,000 deaths, mostly in children in developing countries
Escherichia coli is yet another bacteria that has become multi-drug resistant.
‘Harmless’ strains of Escherichia coli
The 'harmless' strains of Escherichia coli are part of the normal flora of the gut, and can benefit their hosts by producing vitamin K2, and preventing colonization of the intestine with pathogenic bacteria. E. coli and other facultative anaerobes constitute about 0.1% of gut flora.
The healthy human intestine is colonized by as many as 1014 bacteria belonging to more than 500 different species forming a microbial ecosystem of unsurpassed diversity, termed the microbiota. The microbiota's various bacterial members engage in a physiological network of cooperation and competition within several layers of complexity. Within the last 10 years, technological progress in the field of next-generation sequencing technologies has tremendously advanced our understanding of the wide variety of physiological and pathological processes that are influenced by the commensal microbiota. An increasing number of human disease conditions, such as inflammatory bowel diseases (IBD), type 2 diabetes, obesity, allergies and colorectal cancer are linked with altered microbiota composition.
Interestingly, human enteric pathogens are part of a small group of bacterial families that belong to the Proteobacteria: the Enterobacteriaceae (E. coli, Yersinia spp., Salmonella spp., Shigella spp.), the Vibrionaceae (Vibrio cholerae) and the Campylobacteriaceae (Campylobacter spp.). In general, members of these families (be it commensals or pathogens) only constitute a minority of the intestinal microbiota. However, proteobacterial "blooms" are a characteristic trait of an abnormal microbiota such as in the course of antibiotic therapy, dietary changes or inflammation.
In other words, use of antibiotics and nutritional deprivation, can result in bacterial blooms. When the biota is in balance the bacteria do no harm, but once out of balance they can do harm and then even the strains of E.coli regarded as harmless, may become harmful.
E. coli and colicins
Bacteriocins are toxins produced by bacteria to inhibit the growth of similar or closely related bacterial strain(s). The naming of Bacteriocins is generally derived not from the sensitive strain the bacteriocin kills, but instead the organism that produces the bacteriocin. This is because the bacteriocins frequently possess spectra that exceed the bounds of their named taxa and almost never kill the majority of the taxa for which they are named.
Thus the bacteriocins from E. coli are generally called colicins (formerly called 'colicines,') meaning 'coli killers'. So put simply E. coli has an in-built weaponry system that it uses to protect itself. As a piece of weaponry, however, it is a weapon of last resort according to this paper:
Bacteriocins produced by Enterobacteriaceae are high molecular weight toxic proteins that kill target cells through a variety of mechanisms, including pore formation and nucleic acid degradation. What is remarkable about these toxins is that their expression results in death to the producing cells and therefore bacteriocin induction have to be tightly regulated, often confined to times of stress. ….. PMID: 25048159
Bacteriocins are of interest in medicine because they are made by non-pathogenic bacteria that normally colonize the human body. In other words colicins are found in the harmless strains of E. coli described above, and any damage to the mechanism that produces them or releases them, or any damage to the colicins themselves would render the harmless E.coli incapable of defending itself and us.
Antibiotics may wipe out good bacteria and leave us open to infection, as they kill off our intestinal defences, but equally devastating is anything that attacks the colicins, as it has the same effect. We may even have an apparently healthy microbiota, but on closer examination it may be helpless due to its inability to produce colicins.
Given that the harmless bacteria may do battle with the harmful bacteria of the same family, this is of especial relevance, read on.
Pathogenic strains of E. coli
In humans and in domestic animals, virulent strains of E. coli can cause various diseases, for example, gastroenteritis, urinary tract infections, and neonatal meningitis. Virulent strains are also responsible for haemolytic-uremia, peritonitis, mastitis, septicaemia and gram-negative pneumonia. In animals other than humans, virulent strains of E. coli are responsible for septicaemia and diarrhoea in newborn calves, acute mastitis in dairy cows, colibacillosis also associated with chronic respiratory disease, pericarditis, etc. In other words the pathogenic strains can travel all over the body.
Certain strains of E. coli produce potentially lethal toxins. The O157:H7 strain is notorious for causing serious and even life-threatening complications such as hemolytic-uremia and bloody diarrhoea. Severity of the illness varies considerably; it can be fatal, particularly to young children, the elderly or the immunocompromised. Furthermore, antibiotic treatment of children with E. coli O157:H7 infection increases the risk of the hemolytic-uremic syndrome [Ref PMID: 10874060]
If E. coli bacteria escape the intestinal tract through a perforation (for example from an ulcer, a ruptured appendix, or due to a surgical error) or damage and enter the abdomen, they usually cause peritonitis that can be fatal without prompt treatment.
Intestinal mucosa-associated E. coli are observed in increased numbers in the inflammatory bowel diseases, Crohn's disease and ulcerative colitis. Invasive strains of E. coli exist in high numbers in the inflamed tissue, and the number of bacteria in the inflamed regions correlates to the severity of the bowel inflammation.
Enteric E. coli (EC) – that is ones affecting the intestine - are classified in part on the basis of virulence properties. Virotypes include: Enterotoxigenic E. coli (ETEC), Enteropathogenic E. coli (EPEC), Enteroinvasive E. coli (EIEC), Enterohemorrhagic E. coli (EHEC), Enteroaggregative E. coli (EAEC) and Adherent-Invasive E. coli (AIEC)
- ETEC is the leading bacterial cause of diarrhoea in children in the developing world, as well as the most common cause of traveler's diarrhoea.
- EPEC cells also cause diarrhoea, but are also moderately invasive (i.e. they enter host cells) and elicit an inflammatory response. They can also change the intestinal cell ultrastructure due to "attachment and effacement"
- EIEC infection causes symptoms identical to shigellosis, with profuse diarrhoea and high fever
- EHEC can cause bloody diarrhoea, hemolytic-uremic syndrome and sudden kidney failure. It is moderately invasive and possesses a phage-encoded shiga toxin that can elicit an intense inflammatory response
- EAEC bind to the intestinal mucosa to cause watery diarrhoea. EAEC are noninvasive. They produce a an ST enterotoxin similar to that of ETEC
- AIEC are able to invade intestinal epithelial cells and replicate intracellularly. It is likely that AIEC are able to proliferate more effectively in hosts with suppressed or reduced immunity.
As such what we can see is that these bacteria can damage the intestinal wall. By doing so, they open the way for any other number of pathogens to enter the blood stream and travel round the body resulting in infection elsewhere, as such the virulent strains of E. coli may be responsible for any number of illnesses caused by a range of pathogens.
Escherichia coli can produce liver disease, for example
Escherichia coli and Klebsiella pneumoniae are the most common causative pathogens of pyogenic liver abscesses. PMID: 17700198
These are caused by so called ‘Descending infections,’ when E. coli cells enter the from the blood stream.
Bladder and urinary tract disease
Escherichia coli can produce bladder and urinary tract disease, for example
Persistent urinary tract infections (UTI) are often caused by E. coli adhered to urothelium. This type of cells is generally recognized as very tolerant to antibiotics which renders difficult the treatment of chronic UTI. PMID: 21140149
And the bacteria affect other animals besides human beings
We investigated the feasibility of …therapy to combat canine and feline Escherichia coli urinary tract infections (UTIs). PMID: 17959211
Uropathogenic E. coli (UPEC) is responsible for approximately 90% of urinary tract infections (UTI) seen in individuals with ordinary anatomy. In ‘ascending infections’, fecal bacteria colonize the urethra and spread up the urinary tract to the bladder. Because women have a shorter urethra than men, they are 14 times more likely to suffer from an ascending UTI. Descending infections, occur when E. coli cells enter the upper urinary tract organs (kidneys, bladder or ureters) from the blood stream.
In ‘ascending infections’, fecal bacteria colonize the urethra and spread up the urinary tract. As we have seen they go to the bladder, but can also colonise the prostate in males.
In ‘ascending infections’, fecal bacteria colonize the urethra and spread up the urinary tract to the bladder, as we have seen. From there, however, they can then travel to the kidneys. Descending infections, occur when E. coli cells enter the upper urinary tract organs (kidneys, bladder or ureters) from the blood stream.
E. coli is implicated in causing some sorts of cancer
The intestinal microbiota is potentially involved in the development of colorectal carcinoma via various mechanisms. Escherichia coli are commensal bacteria of the human gut microbiota, but some pathogenic strains have acquired the ability to induce chronic inflammation and/or produce toxins, such as cyclomodulin, which could participate in the carcinogenesis process. Here, we analyzed the E. coli population associated with mucosa of patients with colon cancer in relation to clinicopathologic characteristics. …. These findings support that pathogenic E. coli could be a cofactor in pathogenesis of colorectal cancer. PMID: 24334760
Escherichia coli and bacteriophage
Why are such appalling diseases caused by some E. coli strains? Why is it that [assuming we have not destroyed our beneficial bacteria using antibiotics], the bacteria in our intestines seem unable to fight these strains of E. coli, even though they are armed to do so? The answer may lie with bacteriophage.
A bacteriophage is a type of tiny virus. It may attack or colonise bacteria and a number of phages colonise and attack the E. coli bacteria.
The initial step of viral infection is the binding of a virus onto the host cell surface. This first viral-host interaction would determine subsequent infection steps and the fate of the entire infection process. Bacteriophage λ and its host Escherichia coli serve as an excellent paradigm for this purpose. λ phages bind to specific receptors, LamB, on the host cell surface during the infection process. PMID: 23202520
This study investigates the use of lytic bacteriophages … Three collection bacteriophages (T1, T4, and phiX174 like phages) were tested against clinical E. coli isolates …. Based on the lytic spectrum against clinical isolates … the T1-like bacteriophage …. caused nearly a 45% reduction of the bacterial population after 2 h of treatment. PMID: 21140149
The harmless E. coli in our intestines defend themselves and us using the Bacteriocins described above:
We performed three types of experiments to test the hypothesis that abortive infection of T5 bacteriophage in Escherichia coli (ColIb+) is due to internally released colicin…… All possible combinations of colicin production and phage inhibition were found, including mutants that produced no colicin but still inhibited phage production. PMID: 6262536
But the harmful strains appear to have found a way of using the phages as weapons. In other words, although some bacteriophage kill their host, some do not. In some cases, phages use the bacteria as a sort of Trojan horse, in order that it can enter organisms where it can spread and do more harm. But there are bacteria that have learnt how to use phages as weapons.
At one time it appears that many of the harmful strains of E. coli did not use phages, but our overuse of antibiotics, bacterial wipes, disinfectants and so on has meant that the harmful bacteria have increased their use of phages, and in some quite novel ways:
Lysogeny* by temperate phages** provides novel functions for bacteria and shelter for phages. However, under conditions that activate the phage lytic cycle, the benefit of lysogeny becomes a paradox that poses a threat for bacterial population survival. Using Escherichia coli lysogens for Shiga toxin (Stx) phages as model, we demonstrate how lysogenic bacterial populations circumvent extinction after phage induction. A fraction of cells maintain lysogeny, allowing population survival, while the other fraction of cells lyse, increasing Stx production and spreading Stx phages. The uninduced cells were still lysogenic for the Stx phage and equally able to induce phages as the original cells, suggesting heterogeneity of the E. coli lysogenic population. … Our observations suggest that population heterogeneity in phage induction could be widespread among other bacterial genera and we propose this is a mechanism positively selected to prevent the extinction of the lysogenic population that can be modulated by environmental conditions. PMID: 26626855
*The fusion of the nucleic acid of a bacteriophage with that of a host bacterium so that the potential exists for the newly integrated genetic material to be transmitted to daughter cells at each subsequent cell division
** temperate phage Is a bacteriophage which persists through many cell divisions of the bacterium without destroying the host, in contrast to a virulent phage, which lyses and kills its host.
To put this simplistically, bacteria have found a way of spreading the phage armaments to the entire population of bacteria, increasing virulence.
Our harmless E. coli bacteria armed only with colicins is no match for these new pathogens. The virulent strains are much more likely to completely exterminate the harmless strains and go on the rampage in our bodies, and as we have seen above with devastating consequences.
Treatment and prevention
In time we may find that E.coli, once it has entered the blood stream or spread in the body, is capable of causing any number of diseases, not just those listed. As such prevention would seem the best cure.
Practise Basic hygiene - There are obvious precautions related to basic hygiene, washing food, washing hands, cooking food properly. Different strains of E. coli are often host-specific, making it possible to determine the source of fecal contamination, for example, in environmental samples. 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.
Avoid spoiled food - The bacteria can live with or without oxygen so close sealing already contaminated food does not help. Avoid any food where the sealed bags have ‘blown up’, as E. coli uses mixed-acid fermentation in anaerobic conditions, producing carbon dioxide.
Optimum growth of E. coli occurs at 37 °C (98.6 °F), but some laboratory strains can multiply at temperatures of up to 49 °C (120.2 °F). Thus refrigeration will help.
Avoid over sterile environments/boost the immune system - At the same time we need to remember that we do need the harmless E. coli. E. coli found in the gastrointestinal tract normally colonize an infant's gastrointestinal tract, for example, within 40 hours of birth, arriving with food or water or from the individuals handling the child. Too sterile an environment may hinder this.
A balance must be kept of exposure, but coupled with the boosting of the immune system. Feed your intestinal microbiota using food as your medicine. Avoid antibiotics, avoid immunosuppressants, avoid anti-histamines – all serve to depress the immune system or destroy it.
Alter Sexual practises – which also have an impact. Anal intercourse can introduce this bacterium into the male urethra, and in switching from anal to vaginal intercourse, the male can also introduce the bacteria to the female urogenital system.
E.coli and the need for scientific regulation
The long-term evolution experiments using E. coli, such as those begun in 1988, have allowed direct observation of major evolutionary shifts in the laboratory. In one experiment, one population of E. coli unexpectedly evolved the ability to aerobically metabolize citrate. And
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; the use of plasmids and restriction enzymes to create recombinant DNA, became a foundation of biotechnology.
It has not gone unremarked that the increase in unusual strains and illness events seems to coincide with the degree of somewhat uncontrolled research into this bacteria. All commonly used research strains of E. coli for example 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). So there are new strains being invented all the time. It has certainly provided the pharmaceutical companies with a whole host of possible targets and income streams. But there are some ethical scientists around:
The worldwide emergence of antibiotic resistances and the drying up of the antibiotic pipeline have spurred a search for alternative or complementary antibacterial therapies. Bacteriophages are bacterial viruses that have been used for almost a century to combat bacterial infections, particularly in Poland and the former Soviet Union. ….But before bacteriophage therapy can be introduced into clinical practice in the European Union, several challenges must be overcome. ….Can therapeutic products containing natural bacteriophages be categorized under the current European regulatory framework, or should this framework be adapted? Various actors in the field have discussed the need for an … entirely new regulatory framework for the reintroduction of bacteriophage therapy in Europe. PMID: 24500660
One strain, E.coli #0157:H7, produces a toxin called the Shiga toxin. This toxin causes premature destruction of the red blood cells which then clog the body’s filtering system, the kidneys. This in turn can cause strokes due to small clots of blood which lodge in capillaries in the brain. This causes the body parts controlled by this region of the brain not to work properly. In addition, this strain causes the buildup of fluid (since the kidneys do not work) leading to oedema around the lungs and legs and arms. This increase in fluid build-up especially around the lungs impedes the functioning of the heart, causing an increase in blood pressure. Shiga toxins, stx1 and stx2, are important virulence factors of these strains. These genes have been linked to bacteriophages and consequently are susceptible to lateral transmission.
In the bowel, E. coli adheres to the mucus of the large intestine. It is the primary facultative anaerobe of the human gastrointestinal tract. (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.
Food for thought.
If you have become severely infected, the observations provide examples of plant based aids to healing.
References and further reading
- Am J Med Sci. 2007 Aug;334(2):97-105. Comparison of Escherichia coli and Klebsiella pneumoniae liver abscesses. Chen SC1, Wu WY, Yeh CH, Lai KC, Cheng KS, Jeng LB, Wang PH, Lin DB, Chen CC, Lee MC, Bell WR.
- Curr Microbiol. 2011 Apr;62(4):1128-32. doi: 10.1007/s00284-010-9834-8. Epub 2010 Dec 8. Efficacy of a broad host range lytic bacteriophage against E. coli adhered to urothelium. Sillankorva S1, Oliveira D, Moura A, Henriques M, Faustino A, Nicolau A, Azeredo J. 1Department of Biological Engineering, University of Minho, Braga, Portugal. email@example.com
- Environ Microbiol. 2015 Dec 2. doi: 10.1111/1462-2920.13151. [Epub ahead of print] Heterogeneity in phage induction enables the survival of the lysogenic population. Imamovic L1, Ballesté E1, Martínez-Castillo A1, García-Aljaro C1, Muniesa M1. 1Department of Microbiology. University of Barcelona. Diagonal 643. Annex. Floor 0. E-08028 Barcelona, Spain.
- J Mol Biol. 2002 Nov 22;324(2):297-307. E.coli cell-cycle regulation by bacteriophage lambda. Sergueev K1, Court D, Reaves L, Austin S.
- Microbiol Spectr. 2015 Jun;3(3). doi: 10.1128/microbiolspec.MBP-0008-2014. The Roles of Inflammation, Nutrient Availability and the Commensal Microbiota in Enteric Pathogen Infection. Stecher B.
- Res Vet Sci. 2008 Aug;85(1):1-7. Epub 2007 Oct 23. Naturally occurring bacteriophages lyse a large proportion of canine and feline uropathogenic Escherichia coli isolates in vitro. Freitag T1, Squires RA, Schmid J.
- Viruses. 2012 Nov 15;4(11):3162-78. doi: 10.3390/v4113162. Interaction of bacteriophage l with its E. coli receptor, LamB. Chatterjee S1, Rothenberg E.
- N Engl J Med. 2000 Jun 29;342(26):1930-6. The risk of the hemolytic-uremic syndrome after antibiotic treatment of Escherichia coli O157:H7 infections. Wong CS1, Jelacic S, Habeeb RL, Watkins SL, Tarr PI. 1Children's Hospital and Regional Medical Center and the University of Washington School of Medicine, Seattle 98105, USA
- Clin Cancer Res. 2014 Feb 15;20(4):859-67. doi: 10.1158/1078-0432.CCR-13-1343. Epub 2013 Dec 13.Colonization of the human gut by E. coli and colorectal cancer risk. Bonnet M1, Buc E, Sauvanet P, Darcha C, Dubois D, Pereira B, Déchelotte P, Bonnet R, Pezet D, Darfeuille-Michaud A. 1Authors' Affiliations: Clermont Université, UMR 1071Inserm/Université d'Auvergne; Institut National de la Recherche Agronomique (INRA), USC-2018; and Centre Hospitalier Universitaire, Clermont-Ferrand, France
- Arch Immunol Ther Exp (Warsz). 2014 Apr;62(2):117-29. doi: 10.1007/s00005-014-0269-y. Epub 2014 Feb 6. Call for a dedicated European legal framework for bacteriophage therapy. Verbeken G1, Pirnay JP, Lavigne R, Jennes S, De Vos D, Casteels M, Huys I. 1Laboratory for Molecular and Cellular Technology, Burn Wound Centre, Queen Astrid Military Hospital, Brussels, Belgium, firstname.lastname@example.org
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