The E. coli mystery deepens…

And who said spinach was boring?

If the ongoing E. coli outbreak due to spinach has done one thing, it’s highlight the mystery that revolves around Salinas, California:

The sunny Salinas Valley holds a dark mystery: Why, in the past decade, have nine Escherichia coli outbreaks been linked to produce grown here?

It’s still unknown why this fertile land has been hit by what an FDA official calls “significant” crop contamination.

Throughout the picturesque terrain here, questions swirl.

Has cattle waste contaminated irrigation water? Does contaminated soil blow in the wind? Do birds feeding on cow manure carry E. coli?

Is such contamination inevitable to farms so big that the area is known as “The Salad Bowl” to the nation and world? Over 10 years, E. coli outbreaks linked to produce grown here have sickened more than 300 people and killed three.

Not even federal or state authorities know why. “That’s a very good question, and we don’t have an answer to that,” said Dr. David Acheson, chief medical officer for the Food and Drug Administration’s Center for Food Safety and Applied Nutrition. “Certainly huge amounts [of vegetables] are produced there, which is clearly a factor.”

“One thing we know about E. coli is that it’s a resident of the intestinal tract of cattle, and when the cattle manure gets into water systems, it can certainly spread and contaminate anything that the water comes into contact with,” the FDA’s Acheson said.

When investigators inspect a farm, they look at the water supply, farming and processing practices, topography, animal and bird activity, and the hygiene of individuals working the crop, officials said.

A discussion about the internalization of the bacteria by the spinach plant itself (and the bacteria working its way into the leaves) has been hopping on a microbiology listserv I watch, but there hasn’t been any real resolution as to whether that’s really a significant factor, or if authorities simply meant that the E. coli were highly adherent and not easily washed off (as opposed to being physically inside the plant’s leaves). The mystery of why this area seems to be the source of repeated outbreaks of this bacterium seems to be another black box, but it underscores the importance of taking an ecological perspective with disease development–investigating all sources and the interplay between ecosystems, rather than focusing just on the plant or the cattle and being done with it.

7 Replies to “The E. coli mystery deepens…”

  1. I have heard that E. coli O157:H7 does not reside in the intestines of grass fed cattle, rather it is peculiar to grain fed cattle. Could someone clarify this for me?

  2. I am at work now, but I was able to look up a few articles for those who are interested. I have broken these up by topic.

    Note: I took out the http-colon-slash-slash…

    1. The role of cattle – and why they do not become sick:

    Cattle lack vascular receptors for Escherichia coli O157:H7 Shiga toxins
    Ingrid M. Pruimboom-Brees, Tim W. Morgan, Mark R. Ackermann, Evelyn D. Nystrom, James E. Samuel, Nancy A. Cornick, and Harley W. Moon
    PNAS | September 12, 2000 | vol. 97 | no. 19 | 10325-10329

    2. The spread of e coli O157 by houseflies:

    Association of Escherichia coli O157:H7 with Houseflies on a Cattle Farm
    Muhammad J. Alam and Ludek Zurek
    Applied and Environmental Microbiology, December 2004, p. 7578-7580, Vol. 70, No. 12

    3. The spread of e coli O157 by wild birds:

    Isolation of Vero cytotoxin-producing Escherichia coli O157 from wild birds
    J.S. Wallace, T. Cheasty and K. Jones
    Journal of Applied Microbiology 1997, 82, 399-404

    4. The role of Phage 933W and the late expression of the toxin:

    Sequence of Shiga Toxin 2 Phage 933W from Escherichia coli O157:H7: Shiga Toxin as a Phage Late-Gene Product
    Guy Plunkett, III, Debra J. Rose, Timothy J. Durfee, and Frederick R. Blattner
    J Bacteriol. 1999 March; 181(6): 1767-1778

    5. Two major types of phages which are involved:

    Phage Types and Genotypes of Shiga Toxin-Producing Escherichia coli O157:H7 Isolates from Humans and Animals in Spain: Identification and Characterization of Two Predominating Phage Types (PT2 and PT8)
    Azucena Mora, Miguel Blanco, Jesús E. Blanco, M. Pilar Alonso, Ghizlane Dhabi,1 Fiona Thomson-Carter, Miguel A. Usera, Rosa Bartolomé, Guillermo Prats, and Jorge Blanco
    Journal of Clinical Microbiology, September 2004, p. 4007-4015, Vol. 42, No. 9

    6. The diversity of phages encoding the Shiga toxin and the implications for such outbreaks:

    Diversity and Host Range of Shiga Toxin-Encoding Phage
    Shantini D. Gamage, Angela K. Patton, James F. Hanson, and Alison A. Weiss
    Infection and Immunity, December 2004, p. 7131-7139, Vol. 72, No. 12

    7. The use of phages to inoculate sheep against e coli which carry O157:

    Effect of bacteriophage DC22 on Escherichia coli O157:H7 in an artificial rumen system (Rusitec) and inoculated sheep
    Susan J. Bacha, Tim A. McAllistera, Doug M. Veirab, Victor P.J. Gannonc and Rick A. Holleyd
    Anim. Res. 52 (2003) 89-101

    8. Other phages carrying the Shiga toxin:

    Nucleotide Sequence of the Integration Site of the Temperate Bacteriophage 6220, Which Carries the Shiga Toxin Gene stx1ox3
    Claudia Koch, Stefan Hertwig, and Bernd Appel
    Journal of Bacteriology, November 2003, p. 6463-6466, Vol. 185, No. 21

    Sequence of the Genome of the Temperate, Serotype-Converting, Pseudomonas aeruginosa Bacteriophage D3
    JOURNAL OF BACTERIOLOGY, Nov. 2000, p. 6066-6074

    9. More on phages and their role in the evolution of bacterial pathogens:

    Phages and the Evolution of Bacterial Pathogens: from Genomic Rearrangements to Lysogenic Conversion
    Harald Brüssow, Carlos Canchaya, and Wolf-Dietrich Hard
    Microbiology and Molecular Biology Reviews, September 2004, p. 560-602, Vol. 68, No. 3

  3. Houseflies, eh? Makes sense. I’ve seen houseflies land on a cow-pie, slurp up god-knows-what, and then land on a nearby plate of fries and a burger to see what else is good to eat. Remains to be seen just how important a vector they are in the current case.

  4. >I have heard that E. coli O157:H7 does not reside in the intestines of grass fed cattle, rather it is peculiar to grain fed cattle. Could someone clarify this for me?

    That’s not exactly correct. There was a big fuss when someone showed that O157 numbers dropped when grain-fed, O157-positive cattle were switched to grass. Then someone showed that O157 numbers also dropped when grass-fed, O157-positive cattle were switched to grain. In either direction, the diet switch knocks the bacteria back until they adjust to the new conditions or a different batch takes over. There may also be some dietary conditions that promote the bacteria, as in Tara’s URL, but it’s not absolute.

  5. Dave S. wrote:

    Houseflies, eh? Makes sense…. Remains to be seen just how important a vector they are in the current case.

    I only mention the flies because: (a) they showed up in the tech lit; and, (b) I like crows and I wanted to deflect the blame they might otherwise recieve. Crows are fairly smart, and they are always in black.

    Seriously, as I see it, the cows appear to play the role of natural host – they carry the e coli O157 at a fairly high level, but lack the receptors for the Shiga toxin and thus do not become sick, instead shedding the bacteria in their fecal material, much like the deer mouse and the hanta virus. (I would assume that this is extremely common.) One could even argue that they have actually benefited over evolutionary time from carrying the prokaryote – as any predators which took down members of their hurd would become sick – assuming the predators still had the receptor and they weren’t particularly careful once they took down their prey.

    In any case, what I find far more interesting is the coevolutionary relationship between e coli and the phages which infect it. One fellow over on Carl Zimmer’s “The Loom” brought up the following article:

    Evolution of Genomic Content in the Stepwise Emergence of Escherichia coli O157:H7
    Lukas M. Wick, Weihong Qi, David W. Lacher, and Thomas S. Whittam
    J Bacteriol. 2005 March; 187(5): 1783-1791.

    It is a quite interesting piece where they were able to largely reconstruct the evolution of e coli and identify not simply the role which phages have played in its evolution, but the role which e coli has played in their evolution by acting as a kind of mixing vessel, similar to that which geese play for H5N1 in some ways I suppose. The authors describe the new phages as chimera, but I prefer the term mosaic – which seems to be more common in literature on phages. In any case, it strongly reminds me of the following classic:

    Evolutionary relationships among diverse bacteriophages and prophages: All the world’s a phage
    Roger W. Hendrix, et al.
    PNAS | March 2, 1999 | Vol. 96, no. 5 | 2192-2197

    As both articles argue, phages are quite modular. While the general structure of phages will tend to be preserved (e.g., the order in which modules of a given kind appear), different modules will be removed then replace by modules which perform essentially the same function. Moreover, with this sort of coevolution, new ecological niches are explored, and e coli is able to adapt, and unfortunately (at least from our perspective) acquire greater fitness, possibly including the ability to survive outside the host for longer periods of time, and achieves greater diversity – along with the phages which infect it.

    This isn’t necessarily the sort of thing one would wish to hear, but understanding the process by which phage and bacteria evolve placed us in a better position to have some say in it. Of course from my own perspective it is fascinating inasmuch as it may give us insight into how we got here.

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