What about E. coli ST131 (part 2); is it foodborne?

Last November I blogged on E. coli ST131, frequently portrayed as a pandemic clone, combining hypervirulence, ciprofloxacin resistance and ESBL production. The question is whether the undeniable high prevalence of this bug among clinical isolates results from its virulence and antibiotic resistance or whether it is just a reflection of carriage prevalence in the general population, without any relationship to virulence or resistance. Two recently published studies try to shed new light on the debate; one bringing in chicken retail meat as the source……

The authors of the first paper did a remarkable study in 2012 in Flagstaff, Arizona, a rather isolated city with 69K inhabitants (from Chicago take route 66 and you’ll get there). They sampled all available brands of chicken, turkey and pork every 2 weeks from 9 major grocery stores in town, and also collected all clinical human E. coli isolates from urine and blood in town, and performed state-of-the-art molecular analyses. Some of their conclusions; “ST131 has become established in poultry populations around the world and meat may serve as a vehicle for human exposure and infection”; “findings support that a nonnegligible subset of community-acquired E. coli ST131 episodes in the USA is foodborne”. Really?

As an intro into the ST131 family: there are several clades (e.g. H30, H22 and more) and many different plasmids that can go through all clades (e.g., ColV). The sampling yielded 1,118 human and 1,923 meat E. coli isolates, and this is the presence of the ST131 family:

Genotype Patient isolates

(n=1,118)

Meat isolates

(n=1,923)

ST131 N=182

(15.3%)

N=25

(1.3%)

ST131-H22 N=24

(2.0%)

N=24

(1.2%)

ST131-H22+ ColV N=6

(0.5%)

N=20

(1.0%)

 

The authors made a strong case that ST131-H22+ ColV was highly prevalent among the 1.3% of all E. coli isolates found on meat, and that this type was found in a “nonnegligible” 0.5% of humans E. coli isolates.  Somewhere else, this is translated into “Scaled up to the US population, half a percent represents 30,000 to 40,000 cases per year of UTIs and kidney infections — but the total number is almost certainly much higher.” Yeah, you’re right, if eating raw chicken would be causally linked to developing UTI. Also possible: someone is at risk for UTI and is infected with what happens to be at the wrong place at the right time. Could be ST131-H22+ ColV, but also any other E. coli type. In that case, the incidence of UTI us not influenced by exposure to contaminated food.

Whether the meat isolates actually came from living poultry cannot be concluded, as poultry was not studied……  (unclear where the claim of “worldwide establishment among poultry” was based on). Criticizers of the relevance of the animal-human transmission route for resistant bugs have been blamed of having conflicts of interest. Might be (not me), but that may also hold for proponents. Four authors of this paper report having patents “pertaining to E. coli clones and/or resistance”.

Final quote on the study “I think this is the first time that we can truly establish the direction of transmission,” “This shows clearly that people are getting UTIs from E. coli that originate in poultry.” Pretty strong.

The second study builds on the – also – fascinating work suggesting that the epidemiology of ST131 results from something called “negative frequency-dependent selection”; in simple terms a new kid on the block being successful as long as it is seen as a new kid, but its advantage is lost when becoming part of the establishment.” Well, new analyses (don’t ask me to repeat the stats…) now point towards a gained capacity of ST131 to survive in an anaerobic environment (the gut), which fits with the observation that ST131 is a highly prevalent human gut colonizer. The gut flora causes community-acquired infections, and, not surprisingly the most prevalent clones will dominate in clinical isolates, even without antibiotic selective pressure.

Pretty sure that many are now looking for ST131 in animal-derived E. coli. The search for the explanation of the ST131 success story will continue.

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One thought on “What about E. coli ST131 (part 2); is it foodborne?

  1. What about E. coli ST131 (part 2); is it foodborne?

    First, I want to give you kudos for your outstanding efforts to translate the scientific literature for the broader public. In this case, however, I have to challenge your responses to our recent work on ST131-H22.

    Quoted from our paper: “ST131 has become established in poultry populations around the world and meat may serve as a vehicle for human exposure and infection”

    Response: This statement is based on our analysis of a global collection of E. coli ST131-H22 genomes from EnteroBase (https://enterobase.warwick.ac.uk/). This analysis suggests that poultry-associated ColV plasmids have been acquired and maintained (for decades) in multiple E. coli ST131-H22 lineages with representative isolates from North America, Europe, Asia and Oceana.

    Quoted from our paper: “findings support that a nonnegligible subset of community-acquired E. coli ST131 episodes in the USA is foodborne”.

    Response: This statement is based on our finding that 0.5% of the UTIs were caused by ColV+ E. coli ST131-H22. Our research team considers these strains unequivocally of poultry-origin. There is no major poultry production in Flagstaff, where the study was conducted, and therefore, little opportunity for direct poultry-to-human transmission. In contrast, there is a lot of raw poultry products sold in the city. Because of these factors, we considered foodborne transmission to be the most likely mode of exposure.

    Blog: “Really?”

    Response: I obviously think so.

    Blog: “Also possible: someone is at risk for UTI and is infected with what happens to be at the wrong place at the right time. Could be ST131-H22+ ColV, but also any other E. coli type. In that case, the incidence of UTI us not influenced by exposure to contaminated food.”

    Response: This assumes that all strains of E. coli are equally capable of causing UTIs. There is a large body of literature showing that this is not the case and members of ST131 seem particularly adept at causing extraintestinal infections. People who are prone to UTI would be at increased risk of infection if they are colonized by ST131. Our study suggests that poultry products is a source of human exposure (e.g., by inappropriate handling, cross-contamination in the kitchen, undercooking, etc.). I don’t think this is a zero sum game. If one could prevent foodborne transmission of ST131-H22, one may be able to reduce the public health burden of these infections. Ideally, in my mind, one would eliminate this strain from poultry flocks and prevent downstream human infections.

    Blog: “Criticizers of the relevance of the animal-human transmission route for resistant bugs have been blamed of having conflicts of interest. Might be (not me), but that may also hold for proponents. Four authors of this paper report having patents pertaining to E. coli clones and/or resistance”

    Response: The patent disclosure that I have with Sokurenko, Keim and Johnson is on diagnostic markers for the pandemic H30 lineage (not H22). I don’t see how the work in this paper, which highlights potential foodborne risks of the H22 lineage, would benefit us relative to this patent, but the disclosures are there for you to interpret how you will.

    Quoted from me: “Final quote on the study “I think this is the first time that we can truly establish the direction of transmission,” “This shows clearly that people are getting UTIs from E. coli that originate in poultry.” Blog: “Pretty strong.”

    Response: I’ll stand behind this quote. ColV+ ST131-H22 are almost certainly poultry-adapted strains. Phylogenetic inference and ColV analyses strongly suggest that the transmission is from poultry to human.

    Lance Price

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