Use of antibiotics in any setting contributes to the emergence of drug-resistant bacteria, and antibiotic use in food animals is no exception, concludes The Pew Charitable Trusts.
The U.S. nonprofit organization has produced an issue brief looking at the role of antibiotics used on farms in the emergence of antibiotic resistance and how resistant bacteria spread to people.
It notes that while the path from antibiotic use in animal agriculture to the subsequent public health risk posed by resistant bacteria is a complex one, the connection is irrefutable.
The briefing document offers a high-level overview of scientific data available to address three key questions:
1. Does antibiotic use on farms and feedlots lead to resistant bacteria emerging?
Yes. There are pathogens such as Salmonella and Campylobacter, which can cause disease in humans, and commensal bacteria – “friendly” microorganisms occurring naturally in the environment that are harmless in isolation but can ultimately share their resistance genes with bacteria that can make people sick. Evidence from both bacteria types has shown that antibiotic use causes resistance.
Numerous studies, including various randomized control studies, have shown that resistant bacteria can, and do, emerge after food animals were exposed to antibiotics, despite resistance not emerging during the studies in all cases. Observational and other studies have generally yielded similar results.
For example, in one randomized control trial, broiler chickens were infected with strains of Campylobacter known not to be resistant to fluoroquinolone antibiotics. Days later, chickens in the experimental group were given the antibiotics, while the control group was not. Flouroquinolone resistance rapidly emerged in the Campylobacter collected from the exposed birds, but not in the non-treated birds.
Commensal bacteria tend to be easier to study than pathogens. Research has shown that on-farm antibiotic use can and does lead to an increase in resistance among commensals, which can then transfer to more harmful bacteria.
2. Are resistant bacteria on farms or feedlots infecting people?
Yes. Resistant bacteria, both pathogens and commensals, pose a risk to humans directly and indirectly.
Observational studies and other types of research confirm that foodborne and zoonotic pathogens can be transmitted from animals to people. The routes of transmission are complex, but have three primary pathways: direct contact with infected animals, food and environmental transmission. There is no way to quantify which route is the most significant.
Randomized trials and observation studies have demonstrated that commensal bacteria from animals can temporarily establish themselves in humans, for instance, when people have contact with animals carrying the bacteria or handle their meat.
Strong scientific evidence further shows that these commensals can and do share their resistance genes with human commensals and pathogens. The presence of antibiotics seems to make exchanges of resistant genes more likely, but it can happen without them.
In one U.S. study, broiler chickens were given tretracycline in feed, and investigators studied its effects on the intestinal bacteria of family working with the chickens and the family’s neighbors. The emergence of tetracycline resistance was traced to the commensal intestinal bacteria isolated from the birds and from commensal bacteria from workers on the farm. Resistance clearly emerged after tetracycline use on farm, and was more common in the bacteria from exposed farm family members than from their neighbors.
3. Are infections with resistant bacteria worse than if the bacteria were not resistant?
Yes. Strong scientific evidence demonstrates that infections with resistant bacteria are leading to worse outcomes for affected people than similar infections with non-resistant strains.
The degree to which infections with resistant bacteria are worse than those with non-resistant strains appears to differ by pathogen and drug. These differences may, for instance, be the result of a delay in starting effective treatment, or administration of a second choice antibiotic. If first choice drugs have become ineffective and, in some cases, resistant bacteria may “co-select for other traits that make them more dangerous to humans, for example, more likely invade the bloodstream.”
Complexity of emergence and spread
Pew notes that the molecular processes by which resistance emerges, spreads and potentially disappears are complex.
Some resistant genes occur naturally, fully independent of exposure to antibiotics.
Additionally, not every antibiotic works against every type of bacterium. For instance, an antibiotic may be effective only in killing bacteria with a certain type of molecular structure, leaving those without that structure unaffected.
Bacteria can acquire antibiotic resistance through various mechanisms. It may be acquired sequentially, and how quickly this occurs depends on several factors, including the bacterium type, the negative effect any changes have, and the nature of antibiotic exposure.
However, bacteria can also quickly develop resistance when they share their resistance genes. Bacteria can also share several genes at the same time, including those that confer traits unrelated to resistance, which can complicate resistance dynamics through a process called co-selection.
In co-selection, resistance genes are physically linked to genes carrying other traits. This can cause bacteria no longer exposed to antibiotics to retain their resistance properties. Because of this, resistance may appear or disappear significantly faster in some situations than in others, and perhaps not at all during a period of study.
