For some time now, the worldwide food supply has been under attack by a bacterium we know well as a generally non-trouble-making resident of the human colon (Escherichia coli), which has lately been possessed of a terrible “new” weapon in the form of Shiga toxin. We call this beast “Shiga toxin-producing  E. coli” (STEC). We wonder where it came from and why it was sent to plague us. However, E. coli has its problems too. It serves as prey to a number of viruses (bacteriophages). Most bacteriophages use the E. coli cell to make new virus particles, killing the infected bacterium in the process. This is called a lytic cycle. There is another, much more sinister pattern of bacteriophage infection termed a “lysogenic” cycle.  Once inside the host cell, lysogenic viral DNA can integrate itself within the chromosome of the host and stay there, dividing whenever the bacterial chromosome divides. To see a video of bacteriophage attack upon a host bacterial cell, click here. To see the lysogenic and lytic cycles compared, click here. People may prefer to measure the prevalence of STEC rather than the toxin carried by STEC. Such a result could be arrived at using relatively simple and inexpensive tools with a theoretical analytical sensitivity in the range of parts per trillion. By comparison, a chemical or biochemical test run at an analytical sensitivity of parts per trillion, usually involves a roomful of equipment that is expensive to acquire, expensive to maintain and operated by highly-trained personnel who want not just a good salary, health care, vacations and coffee breaks, but who also want to be loved. Several investigators engaged in the study of STEC have remarked that they did not find this organism to be particularly invasive. This finding is consistent with the notion that enterohemorraghic colitis and hemolytic uremic syndrome is the result of the toxicant and not of the “pathogen” carrying it. The premise that STECs are not so much pathogens as carriers for a very potent toxin and that therefore they are not so much examples of infectious diseases as they are of a potent colonic toxicosis (which develops later into a toxemia) would be more convincing if evidence were in hand showing that these disease states could be attained without the detectable presence of STEC at all. Such evidence exists. For example, the first instance of an E. coli O157 outbreak in Denmark was actually attributed to milk coming from a dairy where it had been pasteurized [1]. This report recalls a previous episode from the UK where the drinking of pasteurized milk resulted in intoxication with Shiga toxin, even though microbiological testing of the milk involved had shown that the milk had almost no live microorganisms left in it [2]. Both of these papers appeared to suggest that the pasteurization process at issue was somehow defective even though no bacterial contamination of the milk was found in either case. Years later, it was discovered that Shiga toxin is sufficiently heat stable to survive the usual rigors of pasteurization [3]. If we know that elimination of the presumed infectious agent does not eliminate the disease, then why should food HACCP plans and clinical management personnel assume that an infectious disease is the issue? A recent paper, “Mouse model of hemolytic-uremic syndrome caused by endotoxin-free Shiga toxin 2 (Stx2) and protection from lethal outcome by anti-Stx2 antibody,” by Sauter et. al [4] showed that hemolytic uremic syndrome (HUS) is clearly the result of an intoxication with Shiga toxin as were the previously mentioned two “experiments of nature,” published three years prior to the date of this review, which describes two critically-important phenomena: (i) hemolytic uremic syndrome can be induced by Shiga toxin alone (no STEC needed) and (ii) passive immunization with antitoxin given early enough in the cycle can cure the disease so many previous authorshave said is incurable. The phenomena observed by Sauter et. al by no means constitute the first instance of HUS induction by Shiga toxin alone. Nevertheless, this paper and others of its kind are not merely some arcane addendum to the story of STEC “infection.” They are, in fact, the tail that wagged the dog. They tell us, with convincing clarity, that HUS may be contracted without the help of any infectious agent at all. All that is necessary is the toxin, although other bacterial components (such as the lipopolysaccharide – LPS) may either increase or suppress the activity of the toxin depending upon the details of their administration. Sauter et al. found that a one nanogram dose, given at day zero, day three and day six was sufficient to induce HUS in mice on day eight (and without showing signs of neurological damage). Now a mouse only weighs about twenty grams.  So, the level of the Stx2 intoxicant was actually quite high (50 nanograms per kilogram repeated three times). It was found that a single five nanogram dose killed the mice outright, but not from HUS.  Rather, the mice died from neurological damage. Because of the way the dose was administered, these results could only be possible if Shiga toxin was able to, unaided, cross the peritoneal membrane to penetrate the blood (from where it could easily cause HUS). Such results also suggested that Shiga toxin was able to quite effectively move across the blood-brain barrier to cause its lethal effects on brain function. The “conventional” view held by the U.S. Department of Agriculture and its food safety arm, the Food Safety and Inpection Service, as deduced from actions they have taken and the statements they have made, is that a bloody stool followed by HUS is the result of an infectious disease caused by STEC. If one accepts that view, then one is obliged to consider all the STEC variants as agents of infectious disease (adulterants) and seek to identify and control their living presence in meat and other foodstuffs.  Holding this viewpoint is inconsistent with reports that HUS may be caused without the benefit of STEC at all. Those who hold the infectious disease viewpoint must pay attention to and explain how these observations square with the concept of STEC as an infectious agent. These reports, published in peer-reviewed literature, should be neither ignored nor dismissed. The other viewpoint is that STEC is a relatively noninvasive enteric bacterium, which has lately been hijacked into carrying a very dangerous toxin. This toxin is able to cause the observed sequelae (including HUS) all by itself, which must mean that STEC, while certainly a carrier of this toxin, is not a disease-causing agent as such.  STEC merely carries its stx1 and/or stx2 containing prophage payload into the colon, where it may even reproduce somewhat. However, any STEC’s most salient role is as the victim of the deadly prophage it carries. When that prophage goes lytic, i.e. reproduces as a separate entity within the cell it not only destroys most of the population of its carriers but, in the process, generates the release of sufficient quantities of a deadly poison to the environment where the carriers once resided. The sequelae of that release are bloody stool, the result of a toxicosis of the colon, which then may (or may not) lead to a general toxemia (of the blood). Once that toxin is in the blood, it attacks the kidney merely beca use the cells there happen to be much more sensitive to this toxin than other organ tissues in the human body.  We recognize this result as HUS.  I am unaware of even one report making the claim that any STEC ever caused a septicemia (bacteria in the blood) in those it made ill. This point would seem to confirm the observation that STEC is not very invasive. Whichever viewpoint one subscribes to, it seems clear that E. coli (STEC or non-STEC) should not be tolerated in meat. Of course, good, sanitary manufacturing processes should be followed in the slaughterhouse. Regardless, meat must be pasteurized. Radiation is not the answer. Not only would it trigger customer discontent but within current dose limitations it may only be expected to kill about 99.9% of the population present. This level of effectiveness is not adequate. High pressure pasteurization (HPP) can deliver the effectiveness needed (99.999% kill or greater). Some meat producers (e.g., Hormel) are already using this method, as mentioned in their website. This will certainly eliminate any O157 or non-O157 STEC “adulterants” from meat. However, the possibility left open by treating STEC as an infectious agent and “adulterant” is the possibility that eliminating this so-called “pathogen” through pasteurization without testing for contamination by Shiga toxin may still leave meat unsafe to eat and consumers at risk for HUS. The Centers for Disease Control and Prevention (CDC) has already provided a method with which to measure ricin, a toxin with the same mode of action as Shiga toxin, by use of a clever synthetic substrate for N-glycosidase activity [5]. If we find Shiga toxin in meat, we must have a way to deal with it.  Reliance upon cooking by the consumer does not seem like a good idea. Shiga toxin is a protein and enzyme we already know will survive conditions that pasteurize (HTST) milk. We already have experience trying to cook other protein poisons, such as prions. We know the process often ends in failure. Part of the problem is that while the polypeptide chains of an enzyme may be denatured by heat, we know that often, such denatured polypeptides may autonomously re-fold themselves so as to recreate the very enzymatic activity we were trying to destroy. Recently, it has been shown that Shiga toxin triggers inflammation through interaction with the complement cascade. Block the complement cascade and one ameliorates HUS. It so happens that there is already a drug that does exactly this (Eculizumab – trade name Soliris) [6].  Designed by gene jockeys and cloned for relative ease of manufacture, this drug is a synthetic antibody fragment. It is currently undergoing clinical trials as a treatment for HUS. Food manufacturers, however, may want to hold off on their collective sigh of relief that a “cure” for HUS has been found and that consequently HUS is not as dangerous as it is now when there is nothing even resembling a cure.  Forbes magazine has calculated that the average yearly course of this drug is likely to cost about $409,500 USD, making it the current title-holder for most expensive drug sold in the U.S. On the other extreme (as far as cost is concerned) is manganese [7]. Nodules comprising up to 30% by weight of manganese are said to litter the ocean floor from one end of this earth to the other, so the raw material is there for the taking. This substance has been shown to protect against Shiga toxicosis. The reader will remember that HUS is caused by Shiga toxin after it reaches the blood (toxemia). Nevertheless, if toxicosis of the colon may be controlled by manganese, then perhaps the toxin may be kept from ever getting into the bloodstream to cause a toxemia (and HUS). What is noteworthy about both the Eculizumab and manganese reports is that these presumed curative schema work against the toxin itself. This is an indication (but not proof) that the problem at hand has everything to do with the Shiga toxin and little, if anything, to do with the presumed infectious agent, STEC, regardless of its serotype. The regulatory environment has us currently set to perform handsprings to identify STEC in meat but almost nothing to address the most proximate problem – Shiga toxin.  I think we would be better advised to identify (using a variant of CDC’s analytic method for ricin) and then solve the actual problem: Colonic toxicosis followed by toxemia with Stx1 and/or Stx2. For the full version of this article, which includes more in-depth scientific explanations of observations made above, please visit Food Safety Analysis, LLC’s website. — [1] Jensen, C., S. Ethelberg, A Gervelmeyer, E. M. Mielsen, K. E. Olsen and K. Molbak (2006) “First general outbreak of Verocytotoxin-producing Escherichia coli O157 in Denmark” Euro. Surveill. 11:55-58. [2] Goh, S., C. Newman, M. Knowles, F. J. Bolton, V. Hollyoak, S. Richards, P. Daley, D. Counter, H. R. Smith and N. Keppie (2002) “E. coli O157 phage type 21/28 outbreak in North Cumbria associated with pasteurized milk,” Epidemiol Infect. 209:451-457. [3] Rasooly, R. and P. M. Do (2010) “Shiga toxin Stx2 is heat-stable and not inactivated by pasteurization” International Journal of Food Microbiology 136:290-294. [4] Sauter, K. A. D., A. R. Melton-Celsa, Kay Larkin, M. L. Troxell, A. D. O’Brien and B. E. Magun (2008) “Mouse model of hemolytic-uremic syndrome caused by endotoxin-free Shiga toxin 2 (Stx2) and protection from lethal outcome by anti-Stx2 antibody,” Infection and Immunity 76(10):4469-4478. [5] Kalb, S. R. and J. R. Kalb (2009) “Mass spectrometric detection of ricin and its activity in food and clinical samples” Analytical Chemistry 81:2037-2042. [6] Lapeyraque, A. L., M. Malina, V. Fremeaux-Bacchi T. Boppel, M. Kirschfink, M. Oualhua, F. Proulx, P. Niaudet and F. Schaefer (2011) “Eculizumab in severe shiga- toxin-associated HUS,” New England Journal of Medicine 364:2561-2563. [7] Mukhopadhyay, S. and A. D. Linstedt (2012) “Manganese blocks intracellular trafficking of Shiga toxin and protects against Shiga toxicosis,” Science, 20 January, pp. 332-335, DOI: 10.1126/science 1215930.

  • Donna Lynn

    Great article! It’s all about education and thinking out of the petri plate when it comes to microbiology and food safety. As a microbiologist working in the industry we need to look beyond the obvious. The basics of micro has not changed a lot in the last 75 years but it will if we continue to seek out new thoughts:

  • doc raymond

    A 99.9% kill rate thru irradiation is dissed as not worthy of using by this author. How many lives and kidneys would be saved with this reduction in pathogen levels.
    Toxins are not new, they cause many illnesses and are often present only because the pathogen producing them is present. I must be dumb, but I still don’t want E coli O157 on or in my meat.

  • Doc –
    In the first place, in my article I have already stated: “Whichever viewpoint one subscribes to, it seems clear that E. coli (STEC or non-STEC) should not be tolerated in meat.” So, you and I would appear to be in agreement on this point, albeit for seemingly different reasons. In the second place, decimal reduction rates of steps generally termed “Pasteurization” range from five logs to twelve logs. On that scale, a three log kill just doesn’t cut it. Assume that two samples are challenged with equivalent numbers of bacteria. The survivors of a five log kill will only represent 1% of the survivors of a three log kill. In that light, the answer too your question you raise (“How many lives and kidneys would be saved with this reduction in pathogen levels”) is simply: Not enough. Especially given the sure and certain hit to sales that the resulting irradiation symbol on the package will ensure. Consider that bacteria are very small targets. To kill, ionizing radiation must score a direct hit on the target. If the target is tiny then the radiation dose must be very large. The average absorbed radiation from an abdominal X-ray is about 0.0014 Gy. The approximate absorbed dose needed to kill most bacterial pathogens is 1,500 – 4,500 Gy. The maximum absorbed radiation dose allowed for refrigerated meat is 4,500 Gy. New methods of Pasteurization are out there, meat producers should make use of them. What is not out there is the sort of “safe haven” that has grown up around old “High Temperature Short Time” (HTST) Pasteurization methods, wherein one only had to heat to such and such a temperature and hold that temperature for a given time and your food product could be labeled “Pasteurized.” Meat producers will have to validate for themselves not just the operation of whatever kill step they choose but also its effectiveness. In the third place, pathogens are pathogenic precisely because they are invasive, something STEC is not. The danger in considering STEC a pathogen, as we now do, is that we will think that elimination of this presumed “pathogen” from a food product (though Pasteurization) will make it safe. Two papers I have cited in my article strongly suggest otherwise – that product essentially devoid of microbial life can still cause HUS. I have tried to say that the problem with STEC lies in its capacity to deliver Shiga toxin. We know that the lysogenic prophage carrying the stx1 and/or stx2 genes within a STEC constantly monitors the health of its host. If it sees its host losing its good health, the prophage comes out of lysogeny, enters the lytic cycle and hurries to make both new phage particle components and Shiga toxin. It therefore seems entirely possible to me that a Pasteurization step might just induce any STEC resident in the product being Pasteurized to generate Shiga toxin. The same reasoning explains why antibiotics cannot be used to treat STEC exposure. This point requires checking, something not likely to happen so long as we continue to think of STEC as a “pathogen” and then assume that elimination of this presumed “pathogen” is all that is required.

  • microguy

    Dr. “Mike”,
    I am genuinely interested in this well written article and your perspective. At which sector of the food continuum do you feel there would be such a risk of this occuring? If we consider the production side,it would seem that there would have to be a significant prevalence of STEC in incoming cattle lots (summer months perhaps?) to increase the amount of carcass contamination needed for STEC to produce enough STX on the meat product to even begin to translate into a public health threat (would also likely be indicated early on by failures in HACCP CCPs?). Considering diluting effects, temperature, etc… throughout production and the inhospitable environment resulting from organic acid, chilling and other interventions, it does not seem very likely or plausible that toxin levels could accumulate to a level that would result in HUS illness. So the organism would have to be present for toxin accumulation in a single product to reach levels high enough to physiologically harm the consumer and induce HUS.
    Additionally, foodborne STEC outbreaks resulting in HC or HUS (that I am aware of) always result in either isolates from clinical stool samples with viable STEC or food samples with the viable organism allowing PFGE tracing (infectious disease). The toxin=illness without microbial presence scenario does not seem like a producer problem and therefore not affecting perspective on how STEC is handled. That said, I agree that STEC serogroups are mostly transporters of the actual problem, the prophage and AB protein toxin (STX)product, and we will continue to see emerging serogroups carrying them and causing illness. Therefore regulating them all as “adulterants” can only result in devestating blows to the industry. After all, you cannot regulate nature out of existence…nature will win every time.
    I can visualize this scenario occuring due to abuse of a product at the foodservice level, where a temp abused product like ground beef (containing an STEC because no intervention at the producer level is 100% efficacious)could be left to proliferate with subsequent toxin generation. The product could then be cooked (no viable organism remaining to be isolated from a clinical stool, but potentially high enough toxin levels to result in illness???
    Also,what are the implications with extending your perspective to fresh produce STEC outbreaks resulting in HC and HUS?
    More focus (and perhaps incentive or responsibility) needs to be placed into the pre-harvest environment and the post-production foodservice and consumer theatre. It would be ideal to reduce the levels of the STECs carrying the prophage before they ever even enter the plant, letting plant interventions add to the reducing effects and hopefully, just hopefully…one day distribute a product that individuals cooking said products can hardely screw up. But that would equate to a utopia, a place that apparentely certain litigators and regulators, etc… believe is actually achievable…. I remain unconvinced that there is a possiblity of creating a natural and completely sterile animal based protein source that any consumer would desire to eat.
    If I am grasping your concept correctly, by definintion a pathogen results in disease to its host. Because the HC and HUS are largely a result of the STX toxin, neither the bacteria or prophage would be a pathogen and this would be a toxicosis and not an infectious disease. However, the toxin will not be present without first having been produced by the relationship of the prophage and bacterial cell. In this sense, STEC could be similarly viewed to Staph aureus. However, STEC, through Type III secretion and associated virulence factors, results in inflammation and morphological change to the epitheleal cells that may not be “highly invasive” but are certainly not characteristic of bacteria that are normal resident flora. So…infectious disease or toxicosis? For now, I continue to lean toward infectious disease as the STEC organism will be intimately close to its victim.
    Thank you for such a thought provoking piece.

  • doc raymond

    The toxins from strains of Staph aureus can also make one sick from eating food contaminated with it whether the Staph is alive and present or not. That is not the point. Eliminating or killing E coli O157 will reduce illnesses, just as we are seeing in the annual reports of illness from foodborne pathogens released by the CDC. Industry has done a good job with multiple interventions. No one intervention alone will protect us, and none will give an 8 log reduction. But add them up together and we can save lives. Will the public buy irradiated meat? They already do and most don’t even know it. The ones blocking the way don’t eat much meat, if any, and simply want slower line speeds as a way of reducing contamination and driving up the cost of meat so we will consume less.

  • microguy

    I am in complete agreement that industry has done an excellent job in contributing to the reduction in O157 incidence that is reported in CDC’s MMWR annual FoodNet data report. However,as interventions appear to have been effective in reducing O157, now we have the new rule for the non-O157… and the interventions “should be as effective against the non-O157 serogroups”, yet, there is no conclusive evidence supporting this, not to mention that serogroup is broader than serotype. For all we know, they could be filling a niche replacing the decline in O157? While the hurdle concept to multiple intervention throughout production is effective in reducing DETECTABLE pathogen, I have heard reports that this additive effect is not always observed as factors inbetween hurdles can vary. I think the overall point her is that, no interventions placed in pre or post harvest and their additive effects will be 100% efficient in killing the organims, the potential for illness still falls with the responsibilty of those handling and preparing the foods, though the processors are the ones held liable.

  • Microguy –
    I have grouped your specific questions into the five sections given below, but, before I attempt to answer these, let me say that when I had first written on this topic, it was my intent to produce an argument intelligible to the layman. However, I soon found myself with some 12,000+ words. I asked several extremely patient people to review this article for me and received the overwhelming opinion that I had failed miserably in my quest for simplicity. Far from being a suitable read for the layman, this article was judged to be 24 pages of very pointy-headed text. I then excerpted this article into what I considered to be a “short” version currently available from the link to my website. That version was cut nearly in half to yield the piece published in Food Safety News. Much detailed argument was, of necessity, left behind. I expect to expand and assemble the full, “pointy-headed” version into an eBook that may be ready for distribution this Fall. I hope interested persons will send me an email ( so I may advise them of availability.
    1. At which sector of the food continuum do you feel there would be such a risk of this occurring?
    This is an excellent question. I agree with you when you say that on the production side, it would seem that there would be a significant STEC prevalence among cattle incoming to a CAFO. Once within a CAFO bovines spending the last 150 or so days of their lives within a CAFO may be expected to be stressed and acquire additional STEC. Indeed, there is even the speculation that STEC may actually be an evolutionary adaptation for bovines in a CAFO because the N-glycosidase activity which allows the Shiga toxin to cause as much damage as it does may actually protect the bovine against bovine leukemia virus, given that the uptake of toxin into cells is much less effective in the bovine than it is in humans. This would tend to spread STEC around the feedlot. We already know that ingestion of as few as 10 – 100 STEC cells is said to be sufficient to cause a problem for humans. Humans don’t seem to like CAFOs very much. They are said to smell badly and to be a source of noxious dust, which the wind spreads hither and yon, presumably laden with STEC and allergens. In spite of all this, it seems positively incongruent that I have yet to hear of even one person who either works at a CAFO or the adjacent slaughterhouse or who lives in close proximity to such a facility contracting HUS. One would expect that the CAFO and slaughterhouse would be an epidemiological focus point of STEC distribution. Someone needs to explain to me, at least, why that does not seem to be the case. On the other hand, no one is ever going to find a thing nobody looks for. Has anyone ever checked for the presence of Shiga toxin (not just STEC) in bovine stock held in a CAFO and in the slaughterhouse and any adjacent preliminary processing facilities? If so, please let me know.
    It is true that STEC may be isolated from stool samples of patients presenting with diarrhea. However, by the time HUS begins to develop, any STEC that may have been present initially are long gone and we know that they did not migrate to the bloodstream because I have yet to learn of any STEC septicemia associated with HUS. I agree with you that the microbiological procedures (at least those used by FSIS) associated with testing for all the STEC variants now considered “adulterants” are not for the under-trained and may constitute a cost added on top of the (as yet unknown) cost of the current Midwestern drought and its effect upon corn prices. The price of meat may be in for quite a ride. If testing (for STEC) remains a significant fixed cost against a wildly fluctuating price of goods, then there is the risk that profitability may take a hit. Both producers and processors should note that the CDC method for measuring N-glycosidase activity, while it does involve rather expensive instrumentation, is also much faster than microbiological methods and is amenable to automation. This means that testing for Shiga toxin not only provides data more relevant to the problem at hand, it may be cheaper to use, overall.
    I don’t believe that any sector should be exempt from monitoring. But I also think that microbiological monitoring should be done in concert with Pasteurization. If there is no E. coli, why worry about STEC? Yes, Pasteurization has a cost associated with it, but so does STEC testing. I also think that the further down one is on the “food continuum” the greater is the importance of screening for Shiga toxin. Geneticists have known for some time the ways and means of inducing a prophage to enter its lytic cycle. Obviously some research is needed to test these methods against the STEC we have deemed to be adulterants. Once satisfactory controls are in hand, the best CCP I can think of may be to subject a meat sample to the chosen prophage induction scheme and then test for Shiga toxin. That way we may not have to test for STEC at all and we won’t have to fight evolution (i.e., new serological variants) every step of the way.
    2. …Abuse of product at the food service level
    This is always a danger, given that meat is an excellent growth medium for most bacteria, that abuse of product may lead to unacceptable levels, in that product, of either the carrier (STEC) or the toxin.
    3. Implications for fresh produce STEC outbreaks
    If produce is going to be fertilized by the unsanitized effluvia from CAFOs then I think we will have STEC outbreaks in fresh produce. We already have evidence that viable microorganisms painted on the leaves of young tomatoes can be seen to make their way into the fruit while maintaining their viability. Such internal transfer may (or may not) differ among various produce plant species. Of course, I would think that a tomato is no place for Escherichia coli. What is a Shiga toxin harboring prophage going to make of its host’s sojourn into a tomato? We need data on that point and I have not heard of any on that point.
    4. Creation of a natural and sterile animal-based protein source consumers would want to eat
    Sterility is quite a sweeping claim and may be unattainable as you say, but E. coli free may be doable.
    5. Toxixcosis . . . toxin would not be present without first having been produced by the relationship of prophage and bacterial cell.
    Let us not forget that E. coli is a normal resident of the colon. We already know that if E. coli is able to embed itself into the colonic mucosa, it is able to grow there with a doubling time of from 40 to 80 minutes. Just because an E coli cell picks up a Shiga toxin-containing prophage doesn’t mean that it cannot do what comes naturally to it. The “abnormality” is the Shiga toxin. It would also be well to remember that Shiga toxin genes contained within the STEC prophage are under transcriptional control by two different promoters. One of these makes certain that a low but steady amount of toxin is produced constitutively. The other promoter is not produced until lysogeny ends with the induction of the lytic cycle. This other promoter opens the floodgates of Shiga toxin production. We already know that Shiga toxin triggers inflammation. So, it is all too easy to explain the “ . . . inflammation and morphological change to the epithelial cells” not as an infectious process per se but simply the result of the slow, constitutive release of Shiga toxin from STEC doing what E. coli normally do.

  • Doc Raymond –
    I am disconcerted with the following two of your statements: “Will the public buy irradiated meat? They already do and most don’t even know it.” My concern stems from the wording of the USDA/FSIS final rule issued December, 1999 and effective Feb. 22, 2000 ( on the labeling requirements attendant upon the use of ionizing radiation on meat and poultry:
    a. The final rule requires labeling of irradiated meat and poultry products sold at retail. FSIS is requiring that labeling for packaged meat products irradiated in their entirety must bear the international radura symbol.
    b. For unpackaged meat products irradiated in their entirety, the agency is requiring that the radura symbol and a statement must be prominently and conspicuously displayed to purchasers either through labeling on a bulk container or some other appropriate device.
    c. FSIS is also requiring that inclusion of an irradiated meat product ingredient in any multi-ingredient product be reflected in the ingredient statement on the finished product labeling.
    Meat processors would do well to consider that the reason why limitations on ionizing radiation were set in the first place (and both USDA and FDA appear to use the same limits) is because an excess amount of such radiation is known to induce the formation of toxic compounds (adulterants) in the food being irradiated. This means that quantitation of the adulterants known to be induced by ionizing radiation may be used as a dosimeter by the end consumer (and her attorney) to calculate the total ionizing dosage a given product received. Why would any processor, anywhere along the line between farm and fork want to jump out of the frying pan and into the fire?
    As for Staphyloccus aureus, it is certainly true that this beast produces a number of toxins: (a), alpha hemolysin; (b), beta hemolysin; (c), delta hemolysin; (d), coagulase; (e), hyaluronidase; (f), epidermolytic toxin; (g), leukocidin and (h) enterotoxins (A, B, C, C2, D, E and F). Staphyloccoccus aureus can be quite virulent and intensely invasive, precisely because it is so well equipped. It separates layers of skin (epidermolytic toxin – Nikolsky’s sign). It attacks the blood (coagulase, leukocidin and the various hemolysins, especially beta), it attacks organs (hyaluronidase) and a serious infection certainly can and does go septic (bacteria in the blood). Food poisoning is generally caused by enterotoxins A and/or B. Enterotoxin A is a superantigen capable of stimulating a hyperactive immune response. Enterotoxin B is an incapacitating agent of great interest to the biowarfare crowd. Regardless, an infectious disease, serious though it may be, caused by Staphylococcus aureus can be cured if you kill the pathogen. Treat a patient harboring STEC with antibiotics and you make things worse.
    The point is not about whether examples of exotoxin producing pathogens exist. They certainly do. The point I have been trying to make is that STEC is noninvasive, it does not behave like a pathogen and therefore should not be considered a pathogen. I believe that food safety folk should focus their attention upon the lethal cargo STEC carries – Shiga toxin. To do that, we need to be able to measure its lethal enzymatic activity. A method for doing so exists. We should make use of it.

  • Microguy –
    You are certainly right that a serogroup is broader than a serotype. What is more, the term serogroup can have a rather elastic meaning over time. Bacteria have been around long enough to have become masters of evolution. After all, evolution is what gave us an E. coli prophage laced with stx1 and/or stx2 and made bovine carriage of STEC a protective measure against bovine leukemia virus that makes STEC carriage an evolutionary advantage for bovines, especially in a closely-packed and stressful environment.
    There are many STEC serotypes. As you say, it is entirely possible that as the incidence of one serotype decreases, the incidence of other serotypes increases to fill a “niche” the exact parameters of which we don’t yet understand. It is one thing to take a retrospective look at which serotypes have caused human problems in the past and decide that half a dozen or so merit our special attention. However, there is a risk in making such an assessment. How do we know that the serotypes we believe do not merit attention won’t cause a problem in future? Indeed, how do we know that the same group of serotypes will be prevalent a year or two from now? How often should such reassessments take place? Every time a reassessment is made there are new costs for industry, since new analytic tools have to be made, validated, purchased and put to use.
    On the other hand, we know that all of the STEC serotypes carry a Shiga toxin that has the same enzymatic activity. If we Pasteurize meat sufficiently well that E. coli are nowhere to be found, then we don’t have to worry about which STEC variant may have been lurking about. We do have to worry about whether or not the Pasteurization process itself may not have induced the lytic cycle in any STEC that were present and so left product contaminated with Shiga toxin as they met their demise. I know of no data on this point for any Pasteurization methodology. However, the CDC N-glucosidase assay (as modified for Shiga toxin) will tell us whether or not meat is safe to eat, entirely without regard for the serotype of the prokaryotic culprit. This is a very good thing for processors because if a consumer contracted HUS from eating a meat product the processor had vetted in the manner I propose, I don’t see how that processor could possibly become a whipping boy for either regulators or lawyers. The fickle finger would have little choice but to point elsewhere, perhaps, as you say, to those handling and preparing the foods.
    Food Safety Analysis is a consultancy, not an analytical laboratory. Nevertheless, I believe that I could put together a local group quite capable of measuring Shiga toxin using the modified CDC N-glycosidase activity assay. I am ready to put my proposal to the test. With the right group of collaborators and a robust and well-controlled protocol, we might even, as a group, persuade USDA or FDA or NIH or NSF or someone else to help fund the background work needed to put this proposal in place as a validated and less expensive (as compared with microbiological screening for multiple STEC serotypes) CCP for STEC contamination.

  • doc raymond

    I will cut to the chase, keeping it simple and not hding behind 1,000 words of BS. Wegman’s, Omaha Steaks and Schwann’s all sell irradiated ground beef. The symbol is on the package, but who reads the labels? If people did not buy the product, these companies would not sell it.

  • Doc Raymond –
    Simple works for me. You could have simply dissed the end user by saying that customers don’t read labels. But, you said what you said, which implied to me that labeling rules were not being followed.
    Furthermore, Wegmans is simply running an experiment. It sells both irradiated and non-irradiated beef, giving customers a choice. On top of that, a consumer group has taken Wegmans to task for trying to mislead the public into thinking that irradiated beef is free of E. coli and so may be cooked however a customer likes. Don’t take my word for it, read all about it (
    Your comment goes on to imply that three major companies are successful selling their irradiated hamburger when, in fact, all three (including Schwanns and Omaha Steaks) are running marketing experiments. In fact, unlike Wegmans, Omaha Steaks tells their customers that the irradiation process is “ . . . not meant to replace current food safety practices-it’s meant to supplement them” (
    Like I said, as a Pasteurization scheme, irradiation just doesn’t cut the mustard. The working space between effective and toxic is just too narrow. It may be of use as a partial sanitizing step but that seems too small a benefit considering the labeling requirements. There are better and smarter ways to solve this problem. For that matter, there are also much better uses to which a food processor should put irradiation, especially if she desires that the operation turn a dollar.