Imagine a tiny bacterium lurking in your gut, usually harmless, suddenly evolving into a super-spreader that zips through populations just as swiftly as the swine flu pandemic gripped the world—now that's a chilling wake-up call for global health! But here's where it gets controversial: could this mean we're underestimating everyday bacteria as silent threats, blurring the lines between innocent gut dwellers and potential killers?
Escherichia coli, often just called E. coli, is a type of bacteria that naturally resides in the human digestive system. Typically, it's not a problem at all—think of it as a helpful resident in your gut microbiome. However, groundbreaking new research indicates that certain strains of this bacterium could propagate among people at a rate comparable to that of influenza viruses like the 2009 H1N1 swine flu outbreak.
This is the part most people miss: for the very first time, scientists from esteemed institutions such as the Wellcome Sanger Institute, the University of Oslo, the University of Helsinki, and Aalto University in Finland, along with their partners, have figured out how to calculate the transmission speed of gut bacteria from one person to another. Previously, such calculations were mostly limited to viruses, which spread differently—often through the air or direct contact in ways that bacteria don't always mimic.
The findings, detailed in a study released on November 4 in the journal Nature Communications, delved into three predominant E. coli strains circulating in the UK and Norway. Notably, two of these strains exhibit resistance to multiple classes of antibiotics commonly prescribed. These particular strains rank among the top culprits behind urinary tract infections (UTIs) and severe bloodstream infections in both countries. To put this in perspective, a UTI might start as a simple bladder issue, but if left untreated, it can escalate into something far more dangerous. The researchers argue that improved monitoring of these bacteria could guide public health strategies, potentially averting outbreaks of infections that defy standard antibiotic treatments.
Looking ahead, gaining deeper insights into the genetic mechanisms that enable some E. coli strains to proliferate so effectively could pave the way for more precise medical interventions. For instance, instead of relying on broad-spectrum antibiotics that wipe out both good and bad bacteria (potentially leading to issues like antibiotic-resistant superbugs), doctors might develop targeted therapies that zero in on specific bacterial traits. Plus, the innovative methodology from this study could be extended to other bacterial pathogens, offering a blueprint for tackling a wider array of invasive infections.
To help beginners grasp this, let's break it down: E. coli is a major player in infections globally. While most varieties are benign and part of our body's natural flora, colonizing bacteria like these can enter our systems through everyday interactions—such as a handshake, shared utensils, or even preparing food together. Once inside, if they venture beyond the gut into places like the urinary tract or bloodstream, they can trigger serious problems, including life-threatening sepsis, especially in individuals with compromised immune systems, like the elderly or those undergoing chemotherapy.
Adding to the complexity, antibiotic resistance has emerged as a formidable hurdle in treating these infections. Resistance rates for E. coli vary around the world, but in the UK, over 40% of bloodstream infections caused by this bacterium show immunity to at least one crucial antibiotic. This raises a controversial point: are we overusing antibiotics in everyday medicine, inadvertently breeding tougher strains? And should stricter regulations on antibiotic prescriptions be enforced to curb this trend?
The study introduces a key concept called the basic reproduction number, or R0, which quantifies how many new infections one infected person typically generates in a susceptible population. It's a tool often applied to viruses to forecast epidemic potential—will the outbreak fizzle out or explode? Until now, applying R0 to colonizing gut bacteria like E. coli wasn't feasible because these microbes often live quietly inside us without causing overt symptoms, unlike viruses that always trigger illness.
To overcome this, the team examined colonization data from the UK Baby Biome Study, which tracks how gut bacteria develop in infants from birth—a fascinating example of how our microbiome starts shaping health right from the beginning. They merged this with genomic data on E. coli bloodstream infections from surveillance programs in the UK and Norway, previously compiled by the Wellcome Sanger Institute.
Using advanced software called ELFI (Engine for Likelihood-Free Inference), they constructed a novel model to estimate R0 for these three E. coli strains. The results were eye-opening: one strain, dubbed ST131-A, spreads with the same velocity as viruses responsible for global pandemics, such as swine flu, even though E. coli doesn't rely on airborne droplets for transmission. In contrast, the other two strains—ST131-C1 and ST131-C2, both antibiotic-resistant—don't spread quickly among healthy people in everyday settings. However, they likely accelerate transmission in hospital environments and other healthcare facilities, where vulnerable patients are concentrated. And this is the part most people miss: it suggests that while these strains might not cause widespread community outbreaks, they could spark rapid clusters in places like hospitals, potentially overwhelming healthcare systems.
Having an R0 value for E. coli empowers experts to dissect the factors driving transmission, pinpoint high-risk strains, and craft public health policies to shield those with weakened immunity—such as immunocompromised individuals or newborns.
As co-first author Fanni Ojala, M.Sc., from Aalto University in Finland, explains, “By having a large amount of systematically collected data, it was possible to build a simulation model to predict R0 for E. coli. To our knowledge, this was not just a first for E. coli, but a first for any bacteria that live in our gut microbiome. Now that we have this model, it could be possible to apply it to other bacterial strains in the future, allowing us to understand, track, and hopefully prevent the spread of antibiotic-resistant infections.”
Dr. Trevor Lawley, Group Leader at the Wellcome Sanger Institute and co-leader of the UK Baby Biome Study (though not directly involved in this research), adds, “E. coli is one of the first bacteria that can be found in a baby’s gut, and in order to understand how our bacteria shape our health, we need to know where we start – which is why the UK Baby Biome study is so important. It is great to see that our UK Baby Biome study data are being used by others to uncover new insights and methods that will hopefully benefit us all.”
Professor Jukka Corander, a senior author affiliated with the Wellcome Sanger Institute and the University of Oslo, notes, “Having the R0 for E. coli allows us to see the spread of bacteria through the population in much clearer detail, and compare this to other infections. Now that we can see how rapidly some of these bacterial strains spread, it is necessary to understand their genetic drivers. Understanding the genetics of specific strains could lead to new ways to diagnose and treat these in healthcare settings, which is especially important for bacteria that are already resistant to multiple types of antibiotics.”
Reference: Ojala F, Pesonen H, Gladstone RA, et al. Basic reproduction number varies markedly between closely related pandemic Escherichia coli clones. Nat Commun. 2025;16(1):9490. doi:10.1038/s41467-025-65301-1 (https://doi.org/10.1038/s41467-025-65301-1).
This article has been republished from the following materials (https://www.sanger.ac.uk/news_item/advanced-disease-modelling-shows-some-gut-bacteria-can-spread-as-rapidly-as-viruses/). Note: material may have been edited for length and content. For further information, please contact the cited source. Our press release publishing policy can be accessed here (https://www.technologynetworks.com/tn/editorial-policies#republishing).
What do you think—does this research change how we view everyday bacteria, or are we overreacting to a natural part of our microbiome? Could stricter antibiotic stewardship prevent such resistant strains from emerging, or is it inevitable in a world of global travel and healthcare? Share your thoughts in the comments below—do you agree that we need more funding for bacterial tracking, or disagree that this warrants alarm?
