Antibiotic Resistance has become a topic of major concern, but curiously the idea of surveillance of the specific genetic traits of antimicrobial resistance does not seem to have been folded into our biosurveillance strategy as of yet.
Why is this important? The premise being proposed (not my original thought, although Stuart Levy, founder of the Alliance for Prudent Use of Antibiotics, has been the standard bearer for this emerging field of study) is that these resistance traits arise first in the background flora before they are transferred to pathogens. Very recently, two recent stories have been published that give credence to this idea and emphasize the risk we face from resistant bacteria.
First, there were articles in The Atlantic and Wired Magazine (excellent work by Maryn McKenna) as well as televised coverage suggesting a link between antibiotic use in the poultry industry with antibiotic-resistant E. coli urinary track infections in women. The strongest evidence for this is genomic sequencing showing a very close genetic link between the clinical isolates and the strains isolated from the poultry farms. While not conclusive, it is highly suggestive and raises a concern that merits additional and immediate investigation. While a direct link between antibiotics in the food supply and these infections is hotly contested (unsurprisingly the food industry itself is quite vocal here), there is no doubt at all that profligate antibiotic use is responsible for the meteoric rise of antibiotic resistance.
Second, a recent published article in Science demonstrates identical antibiotic resistance gene sequences in background soil flora and human pathogens. This is a very convincing argument that these traits are readily passed around by horizontal gene transfer from the environment and ending up in the clinic. The use of the hashtag #antibioticresistance is literally screaming on Twitter as a result.
This is one instance where monitoring of pathogens themselves is not going to give sufficient forewarning of the coming problem. A more prudent approach may be to survey for the resistance traits themselves, before they end up in demonstrated cases of human and animal disease with built-in resistance to antibiotics. In the future, we may well take a more broad definition of biosurveillance where traits such as drug resistance, virulence, and toxins are our primary targets rather than a short list of species of interest.
In 2004 Carl Woese coined the term “cosmopolitan genes” (Micro and Mol Bio Reviews, June 2004, p173) to describe “trendy” i.e. useful, horizontally transmitted genes in microbial communities. We have begun to assay our biofilm communities for the presence and expression of certain genes, rather than simply try to infer communal functions from species profiles alone. It seems like monitoring pathogenicity islands and virulence determinants is probably a better strategy than monitoring the pathogens!