How does meat or poultry contribute to the development of antibiotic resistance? Here’s our first story, with NutritionFacts’ Senior Research Scientist, Dr. Kristine Dennis.
According to the World Health Organization, more antibiotics are fed to farm animals to prevent disease and fatten them faster than are used to treat sick people. This can foster the growth of antibiotic-resistant superbugs that can then get transmitted to humans. As the UK’s Chief Medical Officer once put it, “every inappropriate or unnecessary use in animals or agriculture is potentially signing a death warrant for a future patient.”
So, what are they: miracle drugs or pig food? Here’s how Dr. Greger framed the issue in a debate he had with industry representatives, including from the National Pork Producers Council.
“To ask if there’s a question between human drug resistance and livestock antibiotic use is like asking if there’s human-induced climate change, or if there’s a link between smoking and lung cancer. There are a few dissenting industry scientists on one side, but then basically every other scientist on the other. Both opposing camps have scientists on their side, but only one really has science on their side. One can just look at who’s on the sides of this debate. In one corner, you have the World Health Organization, the American Medical Association, the American Academy of Pediatrics, the American Public Health Association, and another 100 medical and public health organizations in the country. On the other side, you have the National Turkey Federation, the National Chicken Council, the Sheep Industry Association, the National Pork Producers. It could not be more stark…”
Previously, Dr. Greger discussed how feeding millions of pounds of antibiotics to cows, pigs, and chickens every year is dangerous because it fosters antibiotic resistance—not necessarily because there’s a problem with antibiotic drug residues getting into the meat itself. But it turns out, he may be wrong.
In 2010, the U.S. Inspector General slammed the U.S. Department of Agriculture for not protecting the American public from the contamination of meat with residual drugs, pesticides, and heavy metals. These drug and chemical residues then find their way to our dinner plates.
But in order to safeguard the nation’s food supply from harmful residues, the USDA, Food and Drug Administration, and Environmental Protection Agency are supposed to test for these contaminants and prevent adulterated meat from entering the food supply. But, based on their review, the U.S. Inspector General found that the National Residue Program is not accomplishing its mission of monitoring the food supply for harmful residues. Regulators hadn’t even established threshold values for many dangerous substances, which has resulted in contaminated meat being distributed to consumers.
What potential effects could the drugs and toxic metals in meat have on people who consume it? Gastrointestinal bleeding, ulcers, allergic reactions, serious nerve damage, severe inflammation, skin cancers, internal cancers, jaundice, kidney failure, neurotoxicity, and even death. Doesn’t cooking destroy the drugs, though? No. No amount of cooking will destroy residues. In fact, in some cases, heat may actually break residues down into components that are even more harmful to consumers.
The Pew Charitable Trusts points out that chemicals that experts agree pose a significant public health hazard are not routinely tested for, while others that pose little risk are routinely included in sampling plans.
The USDA does test for some hazardous drugs though and found that only about one in 260 samples of animal products had drug residue violations. But that suggests more than 100 million pounds of meat adulterated with drugs is served up every year in the United States alone.
Did you know that those eating plant-based have a reduced load of antibiotic resistance genes in their gut. Here’s the story.
There are nearly a million salmonella and campylobacter infections in children 10 and younger each year in the United States. Some of these infections are severe, causing meningitis and death, and requiring treatment with antibiotics. The problem is that there’s an increasing problem of antibiotic resistance among these bugs that threatens our ability to treat them. Part of the problem is that the same lifesaving miracle drug antibiotics are being squandered for use in food animals for things like growth promotion in such unhygienic, crowded conditions, which increases the likelihood that pathogens like salmonella or campylobacter will become resistant––and I’ve done a bunch of videos on that.
There’s another problem. The resistance determinants, the genes that encode antibiotic resistance, may be transmitted from food animals to humans through the food supply. See, most resistant bacteria have mobile genetic elements, like these little circles of DNA called plasmids, that carry the resistance genes that they can pass on to other bacteria, including those in our own gut.
Food animals are, therefore, a reservoir of antibiotic resistance genes, and a potential vector for transmission of antibiotic resistance genes to the human intestinal microbiome. In this study, transfer of an antibiotic resistance plasmid from an E. coli originating from a chicken raised for meat to human gut bugs was assessed by using a model that mimics the human intestines. And, it happened within two hours. This spread of antibiotic resistance genes presents an alarming scenario, a growing concern that antibiotic-resistant bacteria present on food can transfer their resistance genes to the inherent gut microbiome of the consumer. But you don’t know, until you put it to the test. Assessing antibiotic resistance gene loads in vegan vs. vegetarian vs. omnivore gut bacteria.
You’d think the results might be obvious, but antibiotic resistance genes are spread due to manure application on agricultural fields of fruits and vegetables. Yes, massive antibiotic use in animal farming is considered as the greatest contributor to the presence of antibiotic-resistant bacteria (ARB) in food of animal origin: meats, eggs, and dairy. Nevertheless, sewage from treated animals may impact on vegetables grown on fertilized fields, but it was largely unknown whether, and to what extent, antibiotic-resistant bacteria are being transferred to vegetables, and then to the human gut, until now. Researchers looked for antibiotic-resistant genes (ARGs) against sulfa drugs like bactrim, tetracyclines, penicillins and cephalosporins, and streptomycin-type antibiotics. And…both omnivores and vegetarians showed a significantly higher antibiotic-resistant gene load in their guts as compared with vegans.
There wasn’t a significant difference between omnivores and vegetarians, but significantly lower loads in vegans compared to omnivores and vegans compared to vegetarians––the first evidence that a vegan lifestyle is associated with a reduced load of human gut antibiotic-resistant genes, but not the last. Fewer tetracycline resistance genes in vegan guts and more vancomycin resistance genes in the guts of those who eat meat. No surprise, since they found a correlation between tetracycline resistance genes and the intake of eggs, milk, and cheese (I like how there are so many types of milk these days they have to specify “milk from animal source”), and a higher incidence of vancomycin resistance genes was found in consumers of eggs, poultry, fish, and seafood. And vancomycin is one of our antibiotics of last resort, used to treat serious life-threatening strep and staph infections like MRSA.
Despite the links to dairy and eggs, just cutting out meat has indeed been shown to offer an advantage in some studies, as bacteria obtained from meat-eater poop samples showed resistance to a greater number of antibiotics, and carried more tested antibiotic resistance genes compared to the vegan or vegetarian poop.
Finally today, we look at how tainted chicken may result in more than a million urinary tract infections in American women every year.
In my video on antibiotic resistant genes, I explored how more were found in the guts of those who eat meat, dairy, and eggs than those who eat completely plant-based. But does the transfer of bacteria from animal foods in the human gut result in differences in actual clinical outcomes, other than food poisoning, of course? Foodborne bacteria sicken about 350 million people every year, and most of that can be traced to meat, dairy products, and eggs. Besides food poisoning, though, what about “extraintestinal” infections, infections outside the digestive tract? For example, due to pathogenic and antibiotic-resistant E. coli from retail chicken breasts? Infections where, though? The urinary tract.
There’s a type of E. coli called ST131, which is a foodborne uropathogen, meaning it causes urinary tract infections (UTIs)––most of which are just bladder infections, which typically amount to little more than a painful annoyance, but can become invasive and spread up into the kidneys and invade the bloodstream, and end your life. E. coli ST131 emerged explosively in the last 20 years or so “to become the most important multidrug-resistant uropathogen in circulation today.”
Urinary tract infections are caused principally by ascending E. coli infection via an intestine-stool-urethra route, meaning these E. coli that cause UTIs, called extra-intestinal pathogenic E. coli or ExPEC bacteria, start out in the colon, make it to the anus, and then make their way up into the urethra, then into your bladder. How do they get into your intestines in the first place? That’s where the chicken comes in.
The role of poultry-meat, can be to introduce the ExPEC bacteria, allowing it to colonize the rectums of consumers, lying in wait until an opportunity to cause infection presents itself, for example, thrusting from sexual intercourse can introduce the bacteria into the urethra. The time lag between human ExPEC acquisition (in the intestine) and the bladder infection has been the fundamental challenge linking the two. But, we now have strong evidence that a substantial portion of the ST131 strains infecting humans originate from poultry. But they couldn’t tell whether any single infection arose from direct exposure to contaminated poultry, or indirectly from chicken meat from human-to-human transmission––from say a partner who ate some contaminated poultry.
What percentage of human UTIs arise from poultry? Researchers analyzed E. coli isolates from urine samples from patients with suspected UTIs and compared them to the bacteria on retail meat samples in the same region using DNA fingerprinting techniques. They found that about a fifth (21%) of E. coli isolates from suspected cases of UTIs belonged to types found in local retail poultry. Twenty-one percent might not sound like a lot, but E. coli UTIs are one of the most common infectious diseases in the United States, affecting approximately seven million women. So, contaminated chicken may result in more than a million UTIs in American women every year.
This may explain why women infected with multidrug-resistant E. coli reported more frequent chicken consumption––putting them at nearly four times the odds, though frequent consumption of pork was also a risk factor. Wait, is it found in pigs too? Human ExPEC, those extraintestinal E. coli that cause UTIs, have also been identified on pig farms, in pigs, and in retail pork meat––albeit at considerably lower levels than in poultry or chicken meat. So, chicken is riskiest; pork less so, and beef could be considered the safest from a UTI standpoint––since cattle don’t appear to be a reservoir of these particular types of E. coli.
Okay, if meat, including poultry and pork, is the major reservoir for these UTI bacteria, then vegetarians, who avoid meat, should theoretically suffer less exposure. However, no study thus far has examined whether vegetarian diets reduce the risk of UTIs…until now. A prospective study on the risk of urinary tract infection in vegetarians versus non-vegetarians. If around 20% are tied to retail chicken meat, it’s no surprise that eating vegetarian is associated with around 20% lower risk of UTIs, particularly in women. And this association was independent of diseases and predisposing risk factors like hypertension, diabetes, and high cholesterol––meaning it’s not just due to the fact that vegetarians had less diabetes or something.
What about buying organic chicken? Bacteria swabbed from chicken labeled “organic” harbored less antibiotic-resistant bacteria, but no, no less likely to be contaminated with ExPEC UTI bacteria. These findings suggest that retail chicken products in the United States, even if they are labeled “organic,” pose a potential health threat to consumers because they are contaminated with extensively antibiotic-resistant E. coli, including the ones that cause UTIs.
To date, only the Jack in the Box E. coli like O157:H7 are considered food adulterants, meaning it’s not legal to knowingly sell contaminated meat. Why don’t they do the same with the ExPEC bugs, now that there’s such strong evidence they’re infecting so many women? In a survey of retail chicken breasts collected widely across the United States, 14.3% of the E. coli they found appeared to be ExPEC. Given that E. coli can be found in about 90% of retail turkey and chicken products, that would mean the industry would have to dump literally billions of pounds of chicken breasts every year.