by revere, cross-posted from Effect Measure
When a small body of water, say a slow flowing creek or water in a drainage ditch, "goes septic" it starts to stink, often giving off a rotten egg odor (hydrogen sulfide, H2S). This isn't a sign that the water is polluted in the chemical sense of toxic materials. It means that so much organic matter has entered the water that the bacteria there have gone on a food orgy. The initial gluttons are aerobic bugs that need oxygen as a final electron acceptor to generate energy for their needs. When the feasting aerobes use up all the oxygen they die and are replaced by a new set of diners, the anaerobes. These guys can keep eating even without oxygen because they know how to use another common electron acceptor, sulfates, turning them into H2S. Hence the stink. The reason stagnant pools or slow running streams are most at risk when we discharge a lot of "edible" organic matter (like sewage) into them is because they don't get re-aerated faster than the oxygen is being used up. Fast moving streams or artificial aeration is one way to solve that problem and also break down all the organic junk we dump into them.
That's exactly how a conventional sewage treatment plant works. It's loaded with bugs that eat organic material and also supplied with plenty of oxygen. In fact it's set-up to make these beneficial bugs as happy as possible so they can keep eating and eating and eating. Now a new study from the University of Michigan suggests that it isn't only the good bugs that are happy in a conventional treatment plant but the bad ones, too (hat tip reader rustyjewell). They not only eat well but they have sex (of a sort), exchanging genetic material. The result is a gradual enrichment in certain kinds of antibiotic resistant bacteria as they move through the treatment plant:
âWastewater treatment plants are most effective at treating sewage when they have conditions that allow beneficial bacteria to thrive and improve the quality of the water,â said Karen Kidd, a University of New Brunswick ecotoxicologist familiar with the study.âHowever, this study indicates that these conditions can also favor the mutation of some and act as a source of antibiotic resistant bacteria to the environment.â (Andrew McGlashen, Environmental Health News)
The work was done in the lab of University of Michigan microbiologist Chuanwu Xi. Chuanwu and her team collected 366 species of the bacterial species, Acinetobacter, from a treatment plant in Ann Arbor, MI. Antibiotic resistant Acinetobacter isn't as notorious as methicillin resistant Staph aureus ("MRSA") but the species A. baumannii is a really bad actor in hospitals, especially (but not only) among wounded Iraq and Afghanistan veterans (see earlier posts here, here). They followed the Acinetobacter through three stages in the treatment plant (raw influent, second effluent, final effluent) and two in the receiving water, Huron River (upstream and downstream of the plant discharge). Along the way they tested the Acinetobacter for resistance to 8 different antibiotics: amoxicillin/clavulanic acid (AMC), chloramphenicol (CHL), ciprofloxacin (CIP), colistin (CL), gentamicin (GM), rifampin (RA), sulfisoxazole (SU), and trimethoprim (TMP). If you've taken antibiotics recently, chances are you'll see its name on this list. Results?
The prevalence of antibiotic resistance in Acinetobacter isolates to AMC, CHL, RA, and multi-drug (three antibiotics or more) significantly increased (p < 0.01) from the raw influent samples (AMC, 8.7%; CHL, 25.2%; RA, 63.1%; multi-drug, 33.0%) to the final effluent samples (AMC, 37.9%; CHL, 69.0%; RA, 84.5%; multi-drug, 72.4%), and was significantly higher (p < 0.05) in the downstream samples (AMC, 25.8%; CHL, 48.4%; RA, 85.5%; multi-drug, 56.5%) than in the upstream samples (AMC, 9.5%; CHL, 27.0%; RA, 65.1%; multi-drug, 28.6%). (Yongli Zhanga et al., "Wastewater treatment contributes to selective increase of antibiotic resistance among Acinetobacter spp.," Sci. Tot. Env. [abstr.])
What this shows is that resistance to some commonly used antibiotics ramped up fast as the bugs traversed the plant, and while the disinfection of effluent as it was discharged killed most of them, the ones that got through were significantly enriched in antibiotic resistance.
While disquieting, a little reflection suggests this isn't so surprising after all. The antibiotics you take for medical reasons are often not much changed by the time you eliminate them from your body through the sewer system. Add to that the antibiotics from farm run-off in operations that use antibiotics for poultry or cattle and you have a recipe for promoting resistance. The optimal conditions in the treatment plant may also encourage selection. Moreover even without mutation, there are always resistant bacteria around and in the happy confines of the specially engineered microbiological orgy that is a treatment plant there is plenty of opportunity of bacteria to share genes.
One obvious thing to do is decrease antibiotic use, especially for non medical reasons like agriculture. But another would be alter treatment plants so that their effluent is less likely to have live bacteria of any kind. That's a fairly expensive proposition, but maybe somebody will come up with a cheap way to sterilize effluent sufficiently for environmental purposes.
Antibiotic resistance is a major public health problem. Time to find out more how much conventional sewage treatment plants are contributing.