A dangerous E. coli strain has emerged; a small mutation may explain its rise
Neat weaponry
A dangerous E. coli strain has emerged; a small mutation may explain its rise
It's unclear what the mutation does, but it might make E. coli stealthy on lettuce.
Beth Mole
–
May 14, 2025 5:22 pm
|
22
Colored scanning electron micrograph of the rod-shaped, gram-negative bacteria E. coli
Credit:
Getty | STEVE GSCHMEISSNER/SCIENCE PHOTO LIBRARY
Colored scanning electron micrograph of the rod-shaped, gram-negative bacteria E. coli
Credit:
Getty | STEVE GSCHMEISSNER/SCIENCE PHOTO LIBRARY
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Since 2017, a particularly dangerous strain of E. coli O157:H7 has emerged across the country to spark outbreaks, severe disease, and deaths. It spreads in various ways: via leafy greens and contaminated beef, like its relatives, but also recreational waters. Hundreds of people across 46 states have been infected, and health officials have documented at least nine separate outbreaks. One in 2018, linked to lettuce, caused over 200 infections across 37 states, killing five people and causing a severe kidney condition in 26.
Now, a sweeping genetic analysis by researchers at the Centers for Disease Control and Prevention suggests a tiny mutation in one of the bacteria's molecular weapons may be behind the strain's rise. The finding, published recently in the journal Emerging Infectious Diseases, provides insights into this clinically significant plague and its rise to prominence. It also highlights the role of the bacteria's sophisticated military tactics.
The mutated weapon is part of a complex system that E. coli and other harmful bacteria sometimes use called a Type 3 Secretion System. This involves molecular machinery that basically functions like a syringe, complete with a long needle that is poked into the cells of its victims. The T3SS then directly injects a fleet of hostile proteins. Those proteins—called effectors—attack specific targets that collectively disable the host's defense responses and make the host more hospitable for its bacterial conqueror.
The mutation the CDC researchers found was in one of these T3SS effectors, a protein called EspW. Previous research suggests that this effector is responsible for buttressing a host cell's structure during an invasion, keeping the cell from contracting while enabling the bacteria to become attached to it. A related protein in the plant pathogen Pseudomonas syringae, called HopW1, also disrupts normal cellular structure and processes that would otherwise restrict the ability of P. syringae to cause an infection.
Small change
The CDC researchers identified the EspW mutation by comparing the genetic sequences of 729 isolates of the new E. coli strain—dubbed REPEXH01—to genetic sequences of 2,027 other E. coli O157:H7 isolates. Of the 729 REPEXH01 strains, all but two had a single nucleotide deletion in EspW, while the deletion was present in less than 4 percent of the non-REPEXH01 E. coli strains. The finding suggests the tiny change could be a genetic signature of the strain, and its persistence in a key disease protein may offer the strain an advantage.
For now, it's unclear what that advantage might be. The deletion of a single DNA baseshifts the frame of the three-sequence protein code for the rest of EspW. This could result in a shorter protein. It could also cause the molecular machinery that translates the genetic code to slip, leading to proteins of various lengths. In any case, the deletion is likely to result in a less fully functional EspW protein.
The CDC researchers suggest this could help E. coli when it's on lettuce and other produce. For example, EspW might spur an immune response from an infected plant that causes stomata—pores on the surfaces of leaves—to close, blocking the bacteria's ability to invade. Thus, cutting back EspW may help E. coli sneak in—an adaptation in the ongoing arms race between the bacteria and its host. Another possibility is that EspW could function like HopW1, leading to more severe infection in plant tissues, which could lower the chances that those infected leaves are harvested and make it to grocery stores and atop burgers. Thus, cutting back on EspW could help E. coli move to its human victims.
Ultimately, additional research will be needed to understand what's going on. As the CDC researchers conclude: "the role of the single base pair mutation in this strain’s colonization and survival on leafy vegetables could yield valuable insights."
Beth Mole
Senior Health Reporter
Beth Mole
Senior Health Reporter
Beth is Ars Technica’s Senior Health Reporter. Beth has a Ph.D. in microbiology from the University of North Carolina at Chapel Hill and attended the Science Communication program at the University of California, Santa Cruz. She specializes in covering infectious diseases, public health, and microbes.
22 Comments
#dangerous #coli #strain #has #emerged
A dangerous E. coli strain has emerged; a small mutation may explain its rise
Neat weaponry
A dangerous E. coli strain has emerged; a small mutation may explain its rise
It's unclear what the mutation does, but it might make E. coli stealthy on lettuce.
Beth Mole
–
May 14, 2025 5:22 pm
|
22
Colored scanning electron micrograph of the rod-shaped, gram-negative bacteria E. coli
Credit:
Getty | STEVE GSCHMEISSNER/SCIENCE PHOTO LIBRARY
Colored scanning electron micrograph of the rod-shaped, gram-negative bacteria E. coli
Credit:
Getty | STEVE GSCHMEISSNER/SCIENCE PHOTO LIBRARY
Story text
Size
Small
Standard
Large
Width
*
Standard
Wide
Links
Standard
Orange
* Subscribers only
Learn more
Since 2017, a particularly dangerous strain of E. coli O157:H7 has emerged across the country to spark outbreaks, severe disease, and deaths. It spreads in various ways: via leafy greens and contaminated beef, like its relatives, but also recreational waters. Hundreds of people across 46 states have been infected, and health officials have documented at least nine separate outbreaks. One in 2018, linked to lettuce, caused over 200 infections across 37 states, killing five people and causing a severe kidney condition in 26.
Now, a sweeping genetic analysis by researchers at the Centers for Disease Control and Prevention suggests a tiny mutation in one of the bacteria's molecular weapons may be behind the strain's rise. The finding, published recently in the journal Emerging Infectious Diseases, provides insights into this clinically significant plague and its rise to prominence. It also highlights the role of the bacteria's sophisticated military tactics.
The mutated weapon is part of a complex system that E. coli and other harmful bacteria sometimes use called a Type 3 Secretion System. This involves molecular machinery that basically functions like a syringe, complete with a long needle that is poked into the cells of its victims. The T3SS then directly injects a fleet of hostile proteins. Those proteins—called effectors—attack specific targets that collectively disable the host's defense responses and make the host more hospitable for its bacterial conqueror.
The mutation the CDC researchers found was in one of these T3SS effectors, a protein called EspW. Previous research suggests that this effector is responsible for buttressing a host cell's structure during an invasion, keeping the cell from contracting while enabling the bacteria to become attached to it. A related protein in the plant pathogen Pseudomonas syringae, called HopW1, also disrupts normal cellular structure and processes that would otherwise restrict the ability of P. syringae to cause an infection.
Small change
The CDC researchers identified the EspW mutation by comparing the genetic sequences of 729 isolates of the new E. coli strain—dubbed REPEXH01—to genetic sequences of 2,027 other E. coli O157:H7 isolates. Of the 729 REPEXH01 strains, all but two had a single nucleotide deletion in EspW, while the deletion was present in less than 4 percent of the non-REPEXH01 E. coli strains. The finding suggests the tiny change could be a genetic signature of the strain, and its persistence in a key disease protein may offer the strain an advantage.
For now, it's unclear what that advantage might be. The deletion of a single DNA baseshifts the frame of the three-sequence protein code for the rest of EspW. This could result in a shorter protein. It could also cause the molecular machinery that translates the genetic code to slip, leading to proteins of various lengths. In any case, the deletion is likely to result in a less fully functional EspW protein.
The CDC researchers suggest this could help E. coli when it's on lettuce and other produce. For example, EspW might spur an immune response from an infected plant that causes stomata—pores on the surfaces of leaves—to close, blocking the bacteria's ability to invade. Thus, cutting back EspW may help E. coli sneak in—an adaptation in the ongoing arms race between the bacteria and its host. Another possibility is that EspW could function like HopW1, leading to more severe infection in plant tissues, which could lower the chances that those infected leaves are harvested and make it to grocery stores and atop burgers. Thus, cutting back on EspW could help E. coli move to its human victims.
Ultimately, additional research will be needed to understand what's going on. As the CDC researchers conclude: "the role of the single base pair mutation in this strain’s colonization and survival on leafy vegetables could yield valuable insights."
Beth Mole
Senior Health Reporter
Beth Mole
Senior Health Reporter
Beth is Ars Technica’s Senior Health Reporter. Beth has a Ph.D. in microbiology from the University of North Carolina at Chapel Hill and attended the Science Communication program at the University of California, Santa Cruz. She specializes in covering infectious diseases, public health, and microbes.
22 Comments
#dangerous #coli #strain #has #emerged
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