Despite its effects on the skin (read more about this in part 1 here!), E. coli bacteria primary live in animal intestines. There, they produce the bacteriocin, colicin, which supresses the growth of surrounding bacteria and synthesises significant amounts of vitamins, making their presence important for healthy gut function [1, 2].
In this article, we examine E. coli in the gut, discuss contamination and regulation and consider the association between E. coli and antimicrobial resistance.
E. coli and the gut
The E. coli model organism prefers to grow in anaerobic conditions, as in the gut. However, as seen in the evolution experiment, when forced to, this diverse family adapts to live in either aerobic or anaerobic environments [3, 4].
Fortunately, E. coli are mostly harmless and beneficial. Human E. coli strains are classified as commensal microbiota E. coli, enterovirulent E. coli and extraintestinal pathogenic E. coli.
There are six pathogenic E. coli strains, which spread from animals to people, between people and may be carried in water or be found in contaminated food. Let’s break each of them down…
As the name suggests, pathogenic diarrheagenic E. coli strains cause diarrhoea. If you have had an upset stomach when travelling, then it is likely that you were hosting Enterotoxigenic E.coli, (ETEC), which produces toxins (some able to survive cooking) that cause the lining of the intestine to secrete excessive fluid, hence diarrhoea.
Verocytotoxin-producing E. coli (VTEC), meanwhile, is a much nastier diarrheagenic E. coli strain and is often in the news. Sufferers of E. coli VTEC 0157:H7 infection start to show symptoms between one and 14 days after infection and then last for a further 2 weeks. The symptoms are severe pain, bloody diarrhoea, that may – especially in children under 5 years old – develop into haemolytic uraemic syndrome, which can lead to kidney failure and, sadly, death.
Most of the E. coli 0157:H7 pathogenic powers are coded from plasmids. E. coli VTEC strains produce potentially lethal toxins, which bind to specialised surface receptors on human vascular endothelium cells i.e. small blood vessels found in the digestive tract, the kidney and lungs. Other animal hosts of E. coli VTEC do not have these surface receptors and so are not affected by these toxins. Once inside the cell, the verocytotoxin shuts down protein synthesis and (because the toxin is normally ingested), the first sign of infection is bloody diarrhoea [5,6]
Enteropathogenic E. coli (EPEC) is another harmful E. coli strain that infects and causes the deaths of thousands of children per year [7].
Enteroaggregative E. coli (EAEC) is associated with cases of acute or persistent diarrhoea in both children and adults and has been implicated in the development of irritable bowel syndrome (IBS). A 60 MDa plasmid enables it to form its characteristic protective biofilm [8].
More rare are Enteroinvasive E. coli (EIEC) infections which are mainly caused by contaminated water. E.coli EIEC are nonmotile and share many of Shigella spp.’s characteristics. Like E. coli EAEC, E.coli EIEC’s virulence relates to plasmid-borne genes. Released endotoxins cause watery diarrhoea and as the infection spreads it triggers a strong inflammatory reaction, which can eventually result in ulceration [9].
Diffusely adherent E. coli (DAEC) is an extraintestinal pathogenic E. coli and a common cause of urinary tract infections (UTIs). E. coli isolates from skin infections have remarkably similar virulence to E. coli isolates from urinary tract infections and sepsis [10].
Contamination and regulation
Although ever present in the environment and found in low levels in milk, because E. coli are so prolific in the gut, they are considered the most reliable indicator organism for faecal contamination and poor hygiene practices.
Many natural dry ingredients such as henna powders, spices and herbs, are exposed to microbial contamination during pre- and post-harvest, storage and processing, potentially causing frighteningly high levels of E. coli. (In passing, it is worth noting that lemon juice, which is traditionally used to release henna dye, can destroy even the most virulent strains of E. coli [11].)
Reputable suppliers take great care to ensure cosmetic ingredients have zero total plate counts for coliforms and cosmetic regulations stipulate the limits for E. coli as ”absence in 1 g or 1 ml” (European Standard EN ISO 17516:2014) [12].
E. coli should not survive or grow in cosmetics that pass the cosmetics challenge test, a test which is mandatory in many markets. The international cosmetics challenge test standard ISO 11930:2019 and the United States Pharmacopeia standard USP 51 both test preservative efficiency by monitoring the presence of various pathogens – including E. coli – in inoculated cosmetic products. The concentration of these microorganisms is determined at 7, 14 and 28 days after inoculation. Passing the challenge test requires no less than a 2.0 log reduction in microbial concentration from the initial count by day 14, and no further increase in microbial concentration levels at day 28.
Further, as outlined in the European cosmetic product safety report (CPSR), EU regulation 1223/2009 and ISO 29621 stipulate that every cosmetic manufacturer must ensure their cosmetic(s), as purchased, is free from the numbers and types of microorganisms that could affect product quality and consumer health, as well as ensure that microorganisms introduced during normal use will not adversely affect the quality or safety of the product.
However, despite this best practice and the strict regulations in place, studies have shown that E. coli are amongst the dominant microorganisms mostly frequent found in in-use cosmetics [13].
Antimicrobial resistance and preservative tolerance
Counterfeit products and preservative-tolerant bacterial strains may also account for some of the E. coli found in cosmetics.
Increasing antibiotic resistance in preservative-tolerant bacterial strains isolated from cosmetic products is making the scientific community genuinely concerned. Selective pressures from the limited number of preservatives that are allowed in food and cosmetics, combined with extensive overuse of antibiotics globally, is leading to the rise and spread of bacterial resistance [14].
Prolonged exposure of E. coli to antibiotics contributes to the development of antibiotic resistance. A systematic review of antibiotic resistant E. coli strains collected from humans, animals, food and the environment, showed drug resistance is increasing in E. coli throughout the world and in different sources [15].
Unforeseen consequences of the COVID-19 and ‘microbiome friendly’ cosmetics
Logically, with the improvements in hand hygiene through frequent hand washing and the increasing use of alcohol-based hand sanitisers when entering buildings etc., the spread of many harmful microbes will slow down and the incidence of sickness such as those caused by virulent E. coli strains of will fall. The trend for skin microbiota friendly cosmetics must inevitably lead to a more considered use of preservatives and so reduce the pressure leading to preservative-tolerant bacterial strains.
To conclude, E. coli are not always harmful and, indeed, certain strains help keep our guts healthy. However, there are six pathogenic strains whichpose an increasing threat to global health due to the emergence of preservative tolerance and antimicrobial resistance. While regulation aims to combat this by keeping E. coli out of the products we use, there is still a risk of exposure. Another good reason to wash your hands!
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References
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11. Yang, J., Lee, D., Afaisen, S., Gadi, R. Inactivation by lemon juice of Escherichia coli O157:H7, Salmonella Enteritidis, and Listeria monocytogenes in beef marinating for the ethnic food kelaguen. Int J Food Microbiol. 2013 Jan 1;160(3):353-9. doi: 10.1016/j.ijfoodmicro.2012.11.009. Epub 2012 Nov 20. PMID: 23290245.
12. Scientific Committee on Consumer Safety. The SCCS Notes of Guidance for the Testing of Cosmetic Ingredients and Their Safety Evaluation, 9th ed.; SCCS, Ed.; European Union: Brussels, Belgium, 2016; Volume SCCS/1564/15
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