Using the ingredients is primarily a response to patient demand, said (Carolyn Lammersfeld, national director of nutrition at Cancer Treatment Centers of America) but the centers are also "watching the controversy over the nontherapeutic use of antibiotics and their potential to cause resistant strains of bacteria."
The issue is of particular concern for cancer patients, who have compromised immune systems, she noted. "Many also might already being taking antibiotics, so they don't want additional ones in food if they can avoid it," Lammersfeld said.
The drug-free meat is more expensive, but the cost balances out within the budget:
(Diane Imrie, director of nutrition services at Fletcher Allen Health Care in Vermont) estimated that her food costs rose about $67,000 last year when she switched to antibiotic-free chicken from conventional. "But that's also about the same cost as treating a single MRSA infection," she said.
It's interesting to see this story land just as a new paper in Foodborne Pathogens and Disease is making the rounds. The paper (Jiayi Zhang, Samantha K. Wall, Li Xu, Paul D. Ebner. "Contamination Rates and Antimicrobial Resistance in Bacteria Isolated from “Grass-Fed” Labeled Beef Products," doi:10.1089/fpd.2010.0562) compares the bacterial burden in grass-fed and conventionally raised beef and finds no significant differences: equivalent amounts of both drug-sensitive and drug-resistant bacteria in both types of beef.
It concludes, "There are no clear food safety advantages to grass-fed beef products over conventional beef products" — an assertion that's likely to be seized on by those who see no need to change current antibiotic use in agriculture. (For an example of that POV, here's the testimony from last week's House of Representatives hearing by Richard Carnevale, DVM of the Animal Health Institute.)
I suspect though that the paper's analysis doesn't look far enough. Here's one example: the authors found that Enterococcus species in both conventional and grass-fed meat were resistant to chloramphenicol, erythromycin, flavomycin, penicillin, and tetracyline — drugs that are used in agriculture (and that could have been given to the grass-fed animals, which were not guaranteed to have been raised drug-free). But Enterococcus spp. isolates from conventional beef were more frequently resistant to daptomycin and linezolid — which are new-to-market drugs of last resort in human medicine that are not given to animals.
That finding, right there — the migration of resistance to a human-only drug into an organism carried by an animal — signals one of the insoluble problems of overuse of antibiotics. Once created, resistance factors move horizontally among bacteria, from the farm to humans, and apparently in this case, from humans to the farm as well. We have almost no control over their movement, and on the agricultural side, almost no surveillance to detect it, either. That argues for reducing the overuse of antibiotics in human medicine and on the farm.
If this health care coalition's refusal to purchase meat raised using antibiotics helps to enlarge the market for drug-free meat, then it may reduce ag antibiotic use, and therefore the selective pressure that encourages resistant organisms to emerge. That can only be a good thing.
(The paper in Foodborne Pathogens has also been covered by my former colleagues at CIDRAP; here's their link.)
Plan B: Switch over to veggie/myco-based meat substitutes for stay at hospital?
Would appear to take care of most of the concerns...
"That finding, right there — the migration of resistance to a human-only drug into an organism carried by an animal — signals one of the insoluble problems of overuse of antibiotics."
This is not a comment about the paper, per se (which is not a journal we subscribe to); I just wanted to reflect on your comment above. I'm aware that many reports such as these readily supply the observed resistance phenotypes of strains, but commentary on the molecular epidemiology of such resistance cannot be made without addressing the actual determinants and their mechanisms of action (btw, did they do this for those isolates with linezolid resistance?)
Resistance to oxazolidinones, amongst other things has, in the clinic, been seen to be conferred by the determinant cfr, in S. aureus (when not conferred by a chromosomal point mutation). However, this does not mean that there aren't resistance determinates in the environment - entirely independent of clinical or agricultural prophylaxis - that are similarly capable conferring resistance; it's just that they are not the ones seen in the lab/clinic.
If the reference paper 'Sampling the antibiotic resistome' (of soil-dwelling bacteria) is to be built upon, we can anticipate that numerous uncharacterised mechanisms exist for conferring resistance to a/biotics, beyond those that we most commonly see in the clinic. The concern was (and is) that it is only a matter of time before such determinants find their way into the clinic. Although, I should add that I'm also aware there is literature to support a correlation between resistance profile of isolates collected from farms and the drugs used for prophylaxis at the same sites.
However, it cannot be wholly stated that the presence of resistance to 'recent' a/biotics in animals is a direct product of the overuse of such a/biotics without knowing the mechanism by which resistance is conferred. Furthermore, the horizontal transfer of such determinants from soil->animals, or animals->humans may not necessarily result from a/biotic selective pressure, but alternatively via selection for another determinant/virulence factor that is genetically linked with the a/biotic resistance determinant.
I think the persistence of antibiotic resistance in farm isolates, despite discontinued prophylaxis (and thus apparent selection) raises interesting questions. I look at the fitness costs that are imposed on bacteria as a result of the a/biotic determinants they encode. Frequently in the lab we can raise highly resistant strains, but they aren't very 'fit', so in the absence of selection they revert to their ancestral, sensitive forms. Occasionally slightly less resistant forms arise, after multiple generations, which retain their fitness.
Thus, bacteria evolve strategies to mitigate the fitness costs imparted by their a/biotic resistance determinants; indeed, it is the epidemic strains of MRSA that can be said to have overcome such costs.
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