Agricultural antibiotic use and abuse

The agricultural use of antibiotics contributes significantly - perhaps more than use of antibiotics to treat human disease - to selection pressures driving the emergence of antibiotic resistance. As farming has become more commercial, with larger numbers of animals being housed in fewer, more densely populated farms, the role of "agri-antibiotics" has grown. Farmers and veterinarians use antibiotics for three primary reasons: to treat sick animals, to halt the dissemination of infection, and to promote growth. While antibiotics are used at pharmacologic doses to treat or prevent infection in livestock, the common growth promotion-oriented practice uses sub-therapeutic doses, such as less than 200 grams per tonne of feed, for extended periods, with the unintended, but very efficient, selection of resistant bacterial mutants (McEwen and Fedorka-Cray, 2002).

Although the US agricultural industry has not published precise data on the quantity of antibiotics in use, several estimates have been made. An agricultural industry-sponsored group, the Animal Health Institute, approximated that in 1998, 17.8 million pounds of agri-antimicrobials were used, 17 percent of which, they estimate, was non-therapeutic use for growth promotion (McEwen and Fedorka-Cray, 2002). An independent organization, the Union of Concerned Scientists, calculated that annually, in the US, humans utilize 3 million pounds of antibiotics, while the agricultural industry non-therapeutic use is 24.6 million pounds - or 8 times the quantity used to treat human disease (Mellon et al., 2001).

Despite regulations designed to strictly control the quantity of both the residual antibiotics found in food animals at the time of slaughter and spillage of animals' bacteria-laden intestinal contents during slaughter, and processing, antibiotic-resistant bacteria derived from food animals colonize humans and cause human disease. For instance, genetic sequencing allowed the tracing of an outbreak of antibiotic-resistant Salmonella serotype Newport in California from infected patients back to a fast-food hamburger chain, to a meat-processing plant, and finally to the farm where the source-cattle were raised (Swartz, 2002).

Concerns about the ecologic impact of agri-antibiotics are global. Before 1997, European Union (EU) farmers extensively used the glycopeptide antibiotic avoparcin as a growth promoter. Resistance to avoparcin confers cross-resistance to vancomycin, and the agricultural use of avoparcin has been linked to the emergence of VRE in Europe. While glycopeptides seldom had been used medically in Europe in the early 1990s, the presence of significant percentages of VRE carriers in the community suggested a problem. For instance, the former East German Government strictly limited vancomycin use, yet 12 percent of healthy patients demonstrated intestinal colonization with VRE (Bates, 1997).

While European physicians may not have used glycopeptide antibiotics in the early 1990s, the same cannot be said for the European agricultural industry. In Denmark, in 1993, physicians prescribed 24 kg of vancomycin, while farmers used 24,000 kg of avoparcin (Aarestrup, 1995). Not surprisingly, Danish researchers found that chicken farms using avoparcin had a 55 times greater chance of harboring VRE-colonized broilers compared to farms that did not utilize avoparcin (Bates, 1997). Research examining VRE colonization rates among Dutch turkey farmers who used avoparcin provides a circumstantial link between food animal VRE carriage and human colonization. The researchers found fecal samples colonized with VRE from 50 percent of turkeys, 39 percent of turkey farmers, 20 percent of turkey slaughterers, and 14 percent of area residents (van den Bogaard et al., 1997).

Agricultural quinolone use has been linked to increasing rates of quinolone-resistant Campylobacter jejuni, but, unlike VRE colonization in healthy hosts, C. jejuni commonly causes clinical disease. The US first licensed agricultural fluoroquinolone use in 1995. To assess the effects, the Minnesota Department of Public Health studied quinolone resistance rates among human Campylobacter isolates. They found an increase in the state-wide proportion of quinolone-resist-ant C. jejuni, from 1.3 percent in 1992 to 10.2 percent in 1998. In 1997, they cultured quinolone-resistant C. jejuni from 14 percent of chicken parts sampled from 91 retail markets in the state. Using restriction enzyme-based sub-typing, the researchers showed the presence of identical quinolone-resistant C. jejuni isolates from both chickens and humans (Smith et al, 1999). The National Antimicrobial Resistance Monitoring System for enteric bacteria (NARMS) corroborated these findings. In 1989-1990 they documented no cases of quinolone-resistant Campylobacter, while by 2001 19 percent of Campylobacter isolates demonstrated quinolone resistance. NARMS surveillance found that of 180 chicken products tested from three states, 10 percent harbored quinolone-resistant Campylobacter (Gupta et al, 2004).

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