By Naomi Lubick of Nature magazine

The South Platte River system begins in pristine Rocky Mountain streams and flows east through the Coloradan plateau dotted with cattle ranches, sheep pastures, dairy farms — and human wastewater-treatment plants. In the first quantitative survey of a whole landscape, researchers have mapped how human activities affect the concentrations of antibiotic-resistance genes in the watershed.

Amy Pruden of Virginia Tech in Blacksburg and her colleagues tracked two integrons — genetic elements that can be traded by microbes or persist on their own in the environment — called sul1 and tet(W), which confer resistance to sulphonamide and tetracycline antibiotics, respectively. Both classes of drugs are used in animals and humans.

Over the course of a year, the researchers sampled ten sites in the watershed, including both the relatively pristine upstream areas and those downstream of human activity. The team characterized 89 water-treatment plants and 100 animal-feeding operations that feed into the river. The South Platte receives treated waste effluent from places such as Denver, and in February, the driest time of the year, its flow can be dominated by effluent.

Pruden says that sul1 antibiotic-resistance genes were 1,000–10,000 times higher in human-affected sites than in the 'natural background' of more pristine areas of the watershed. There was also a linear correlation between sul1 concentrations and the number and location of wastewater-treatment plants and animals upstream.

But there was no clear correlation between tet(W) and human activity, nor did tet(W) concentrations match previous measurements of tetracycline antibiotics in river sediments that might have led to the development of local pockets of resistance in microbial communities.

The team speculates that sul1 genes are more “promiscuous”, or more readily taken up by bacteria in the environment and spread around, whereas tet(W) is more limited. Mechanical means of transportation might dominate its movement in the environment, such as being attached to sediments.

Background resistance
Resistance genes occur naturally in the environment; prehistoric ice samples show TetM alongside mammoth DNA in 30,000-year-old Alaskan permafrost. That background makes it important to characterize “both the natural occurrence of the antibiotic-resistance genes and the anthropogenic load, and where those genes come from, and it’s good to do it in a quantitative way,” as Pruden’s team did for the South Platte, says Joakim Larsson of the University of Gothenburg, Sweden, who has tracked antibiotics and resistance genes in India and Sweden.

Dana Kolpin of the US Geological Survey in Iowa City says that the findings highlight the complex issue of antibiotic-resistance genes, which will continue to be of concern as treated effluent becomes more widely used in regions that have scarce water resources. But he cautions that although Pruden’s model is helpful in understanding the South Platte system, “you cannot extrapolate to all basins, as all will be unique”.

Pruden and other researchers may have a chance to track these risks soon: she and her colleagues recently completed an unpublished study of wastewater effluent from Flagstaff, Arizona, showing that microbes that might carry antibiotic resistance survive the treatment plant’s relatively thorough methods, and thrive in the pipes that carry the treated effluent to be used elsewhere. The scientists have also detected resistance genes for sulphonamides and another antibiotic in the treated wastewater — which will be turned into snow at a nearby ski resort, in a relatively pristine part of a river basin, later this year.

This article is reproduced with permission from the magazine Nature. The article was first published on October 17, 2012.

6 Comments

1. 1. papadick 06:06 PM 10/17/12

   go figure.

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2. 2. RDFInOP 07:12 PM 10/17/12

   So here is what I would like to know. If we were to completely stop using antibiotics and the trait were not longer necessary, would it ever breed it's way out of the system? Would the trait just be a dormant thing forever? I bet there is someone out there that knows this.
   
   I realize that this is unlikely to happen but one can hope that we will wake up someday and realize that prophylactic use of antibiotics in agriculture is a really bad idea.

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3. 3. papadick in reply to RDFInOP 08:19 PM 10/17/12

   The cessation of prophylactic antibiotic use is, at best, an unrealistic scenario - for many reasons. As for the continued existence of "resistance genes", it depends upon "selection pressure". In the presence of antibiotics there exists a positive selection pressure to evolve resistance to same. The absence of those antibiotics would not - in and of itself - constitute a reason for those genes to de-evolve. It would require some sort of negative selection pressure to eliminate them.

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4. 4. Laroquod in reply to papadick 07:39 AM 10/18/12

   I can't prove it but it is pretty likely that there are deleterious effects to many antibiotic resistance genes. There are natural antibiotics out there -- we didn't event them; therefore, antibiotic resistance would have already been prevalent unless there were some deleterious effect that pushes selection pressure away from it. The introduction of large quantities of artifical antibiotics into the environment changes the equation though; now there are so many antibiotics around that it becomes "worth it" to accept deleterious effects in order to acquire that resistance -- the selection pressure would flip the other way. If the artificial antibiotics were removed from the environment, then it's fairly likely (though entirely hypothetical on my part) that the selection pressure would flip again and antibiotic resitance would, indeed 'de-evolve'.

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5. 5. papadick in reply to Laroquod 12:18 PM 10/18/12

   Interesting hypothesis. It involves however, an unwarranted assumption - that deleterious effects automatically accompany a "desired" effect. That said - there is one graphic example that comes to mind of just such a scenario - sickle cell anemia. Sickle cell is not a "disease" in the sense that the flu or rabies, etc, is an infectious "disease". Sickle cell anemia is an evolved genetic trait (at the hemoglobin chromosome locus) for combating malaria. Malarial parasites (Plasmodium species) cannot survive in sickled cells. In the ancestral environment - Africa - where malaria was endemic - a natural balance evolved: 1/3 of the human population with "normal" hemoglobin - subject to death by malaria. 1/3 of the pop. sickle-cell - subject to death by anemia. AND 1/3 of the pop. heterozygous for normal/sickle - likely to survive long enough to reproduce. There are, indeed, "natural" antibiotics - cerumen (earwax) & spider web (silk), being two good examples. Spider web is well known to back-country hikers/campers as an emergency wound dressing - both for it's binding ability & for it's antibiotic properties. With regard to your hypothesis - it does not follow necessarily that the absence of an agent automatically confers a genetic "flip". Some sort of negative selection pressure must occur or it is likely that the gene alleles will persist in the gene pool. This is why, in the absence of malaria in the USA (may be about to change-global warming) sickle anemia persists in the afro-american community - they brought those genes with them and there has been no negative selection pressure to eliminate them.

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6. 6. bucove in reply to RDFInOP 10:42 PM 10/24/12

   RDFInOP
   
   My understanding is that the metabolic load these genes place on the organism which expresses them precludes their propogation for more than 2 or 3 generations after the evlutionary pressure requiring them is removed

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