Introducing Escherichia coli (E. coli) part 1

Escherichia coli (E. coli) was discovered in faecal samples from healthy individuals by Theodor Escherich back in 1885, who identified it as a key gut microbe. Since then, it has become molecular biology’s most popular model organism and arguably, the most well-known and well-studied bacteria in the world [1].

Key scientific milestones, such as deciphering the genetic code, and breakthroughs, enabling some of the latest cosmetic ingredients to be manufactured through biotechnology, owe so much to this tiny organism [2].

E. coli is a celebrity among bacteria – it is possibly the most well-known bacteria among scientists and non-scientists alike. It has even held Guinness World Records: today it holds the record for the longest time survived in space by bacteria. The record states ”From 7 April 1984 to 11 January 1990 E. coli bacteria cells survived unshielded onboard NASA’s Long Duration Exposure Facility satellite, in low Earth orbit” [3].

Here, we examine how E. coli achieved its celebrity status, the processes it goes through in a day, and how it impacts the skin microbiome.

E. coli… why is it such a big deal?

Well, E. coli is particularly resourceful. Many E.coli strains can produce biofilms when stimulated by factors, such as stress hormones [4], and most are motile due to their flagella that project in all directions. It increases its capabilities by readily accommodating mobile genetic elements through infection by bacteriophages or by acquiring plasmids from other Enterobacteriaceae [5]. These mobile genetic elements can code for factors enabling E. coli to be more virulent and a stronger fighter in the microbiome.

Virulence factors, which make it possible for pathogenic strains of E. coli to evade the body’s immune response or be resistant to antibiotics and preservatives, are of particular concern. There are a wide range of transferable characteristics, which together turn unarmed harmless E. coli into armed and dangerous pathogens and in extreme cases, into agents of death! Most worrying is the speed with which plasmids evolve. Plasmids in bacteria, which contain multiple plasmids, are under tremendous pressure to recombine. Once recombined, recombinant plasmids can generate significant changes in the population. A key step in the evolution of the pathogenic genus Shigella from a non-pathogenic E. coli ancestor, is believed to be plasmid acquisition [6].

A day in the life – doubling, aging and evolution

Under ideal conditions, the rod shaped, gram negative E. coli, just 0.4-0.73 µm, can divide every 20 minutes. While this might not sound like much, a single E. coli bacterium, in theory, could produce up to 72 generations in a day – this amounts to 4,722,366,482,869,645,213,696 individual bacterial cells. Each division is almost, but not completely, symmetric. The original parent cell becomes a weaker non-identical ‘clone’ of the two cells formed by the division. Although seemingly identical to its ’clone’, the weaker bacterium contains slightly different components. Similar asymmetric division occurs when these two new cells divide and in all their subsequent divisions. The weakened cells have slower growth rates and higher death rates. Therefore, a growing colony of E. coli is comprised of a mix of E. coli cells at various stages of weakness and, by the end of the day, the 72 generations can be thought of as an aging community [7,8].

An interesting ongoing long-term evolution experiment started tracking genetic changes in 12 identical populations of E. coli back in 1988 and is still going to this day. The results have shown that all 12 populations increased their growth rates and cell sizes, and each population observed similar rapid peaks of improved fitness followed by an ongoing gradual decline. As with diverse skin microbiome communities, these E. coli cells are constantly competing for resources. As such, logically, the fastest growing of the best adapted cells are the ones that quickly prevail, hence the peak in fitness. Just before the COVID-19 lockdown in March 2020, this experiment had reached 73,500 generations – that’s a lot of cells! Despite E. coli preferentially growing in anaerobic conditions, along with the many genotypic and phenotypic changes that occurred on the way, at some point – between generations 31,000 and 31,300 –the populations had evolved to grow aerobically on citrate [9].

Beyond the evolutionary steps that E. coli go through even within 1 day, a study took an E. coli population limited by nutrients (so as to be in the stationary and death phases) and showed it displayed rhythmic variations with a period of around 24 hours under light/dark cycles and under constant darkness, providing evidence of it having a sense of time [10].

E. coli and the skin

Undoubtedly, without sufficient hygiene, E. coli can be transferred from animal-person and from person-person via our skin – but, as Theodor Escherich supposed all those years ago, skin is not its primary habitat -primarily residing in the gut[11].

Yes, E. coli strains are isolated from skin and from skin infections, confirming its presence [12]. However, levels of E. coli on healthy skin are surprisingly low when you consider the high exposure that certain areas of skin have to gut bacteria as well as its ability to adapt.

Studies show that E. coli can induce keratinocytes to secret the S100 protein, psoriasin, which selectively targets and kills E. coli thereby limiting its own presence in the skin microbiome [13]. When skin is damaged, perhaps from burns, following surgery or due to conditions such as eczema – which is associated with keratinocyte apoptosis – E. coli can cause skin infections such as cellulitis, and on rare occasions in type 1 necrotizing soft tissue infections (NSTIs), where layers within the dermis, subcutaneous tissue, superficial fascia or muscle become infected [14].

Although cellulitis is a common skin and soft tissue infection (SSTI), incidents of cellulitis due to E. coli are unusual and occur mainly in immunodeficient patients, where E. coli first infects their blood (sepsis) before infecting their skin. E. coli isolates from skin infections exhibit a remarkable virulence potential comparable to E. coli isolates from urinary tract infections and sepsis. [15]. Fortunately, like these other E. coli infections, E. coli skin infections can be treated with antibiotics and cocktails of E. coli-specific bacteriophages [16].

In summary, E. coli are far from dull and busily divide and exchange genetic material in order to better survive. As the molecular biologists’ ”lab rat”, E. coli deserves our greatest respect. This record-breaking survivor in space, while able to live in the body without causing any harm, can also be an agent of death.  With its proven impact on the skin’s health, among other regions of the body, it provides another reminder to wash your hands thoroughly to stop the spread of E. coli, as well as other infections.

Read about a day in the life of another bacteria, C. acnes, here and browse the Content Hub for more!

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6. Niu, C., Yang, J., Liu, H., Cui, Y., Xu, H., Wang, R., Liu, X., Feng, E., Wang, D., Pan, C., Xiao, W., Liu, X., Zhu, L., & Wang, H. Role of the virulence plasmid in acid resistance of Shigella flexneri. Sci. Rep. 7, 46465; doi: 10.1038/srep46465 (2017).

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8. Stewart, E.J., Madden, R., Paul, G., Taddei, F. Aging and Death in an Organism That Reproduces by Morphologically Symmetric Division. PLoS Biol. 2005. 3(2): e45.

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10. Fortes-Silva, R., Oliveira, I.E., Vieira, V.P., Winkaler, E.U., Guerra-Santos, B., and Cerqueira, R.B. Daily rhythms of locomotor activity and the influence of a light and dark cycle on gut microbiota species in tambaqui (Colossoma macropomum). Biological Rhythm Research 2016. 47:2, pages 183-190

11. Day, M.J., Hopkins, K.L., Wareham, D.W. et al. Extended-spectrum β-lactamase-producing Escherichia coli in human-derived and food chain-derived samples from England, Wales, and Scotland: an epidemiological surveillance and typing study. Lancet Infect Dis. 2019; (published online Oct 22)

12. Petkovsek, Z., Elersic, K., Gubina, M., Zgur-Bertok, D., & Starcic Erjavec, M. Virulence potential of Escherichia coli isolates from skin and soft tissue infections. Journal of clinical microbiology, 2009. 47(6), 1811–1817.

13. Gläser, R., Harder, J., Lange, H. et al. Antimicrobial psoriasin (S100A7) protects human skin from Escherichia coli infection. Nat Immunol 6, 57–64 (2005).

14. Gallois C, Hauw-Berlemont C, Richaud C, Bonacorsi S, Diehl JL, Mainardi JL. Fatal necrotizing fasciitis due to necrotic toxin-producing Escherichia coli strain. New Microbes New Infect. 2015;8:109-112. Published 2015 Jun 15. doi:10.1016/j.nmni.2015.06.003

15. Sunder, S., E. Haguenoer, E., Bouvet,D., Lissandre, S., Bree, A., Perrotin, D., Helloin, E., Lanotte, P., Schouler, C., and Guillon, A. Life-threatening Escherichia coli cellulitis in patients with haematological malignancies Journal of Medical Microbiology (2012), 61, 1324–1327

16. O’Sullivan, J.N., Rea, M.C., Hill, C., Ross, P.R. Protecting the outside: biological tools to manipulate the skin microbiota, FEMS Microbiology Ecology, Volume 96, Issue 6, June 2020, fiaa085,

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