Here at Golden Rule Honey, we are unabashed fans of the basic research being done by Dr. Nancy Moran and her team at Yale University on the microbes associated with honeybees. Here is the latest study out, and it includes comparisons of the antibiotic resistance of the microbes in the guts of Dee Lusby's untreated bees to those at the Tucson Bee Lab...virtually down the road.

http://mbio.asm.org/content/3/6/e00377-12.full

This work at the Moran Lab is really significant beyond the specific findings. It is the first time that any researchers have been willing to look at the gut microbes of untreated bees separately from those of treated bees. ..the first time that untreated bees have even been considered as something separate that needs to be looked at separately in order to determine any kind of meaningful baseline (seems rather obvious, no?).

In summary, this work shows rather definitively that gut microbiotia is heritable (and very old), and that a line damaged by antibiotics does not return (at least in 25+ years) to its original population. How these populations are affected by other treatments, feeds, and ag chemicals remains to be seen…but Gilliam’s work in the 70’s showed a big change in gut microbal makeup when bees were fed sugar, confined, exposed to 2,4,D, fumagillin, and terramycin (yeasts, molds, and bacteria).

What This Study (and others from the Moran Lab) Showed

• That gut microbes in bees from countries that never used antibiotics have a very low copy rate of antibiotic resistance in their gut microbes [this is to say that the genetic traits of antibiotic resistance occur only infrequent within the population].
• That Bees From Dee Lusby’s operation have levels almost as low as those from countries that never used antibiotics…lower than “feral” bees from Utah…much lower than bees from the Tuscon Lab nearby (that are 2 years without antibiotics)….much, much lower than bees established from commercial packages...but they also showed _kinds_ of antibiotic resistance (In small amounts) that were not found at all in countries that had never used antibiotics.
• That some of the actual genes responsible for the antibiotic resistance are the same ones found in other areas of agriculture, and the same ones found in antibiotic resistant AFB. it appears that these traits are able to "jump" between species of bacteria. It is not clear where these traits originated, but they certainly share a common source.

What is Significant

• The honeybee microbial community is very diverse, and presumably selecting for only the antibiotic resistant individuals greatly reduces this diversity (a bottle neck selecting only for the antibiotic resistant individuals). In the buildup period following wiping out all the non-resistant variations, millions of years of co-evolution are thrown out the window.
• Remember that in parallel to selecting _for_ antibiotic resistance, since you are placing the microbial culture into an environment where antibiotics are used to suppress pathogenic bacteria, any pressure on the community to suppress these pathogens is removed…you are now selecting _against_ traits of bacteria that can suppress EFB, AFB, etc. when antibiotics are used.
• Thusly rebuilt communities lack the continuum of diversity inhabiting the continuum of niches that exist throughout the digestive tract and throughout the superorganism…they can’t possibly be as efficient as the undamaged version….and remember…these communities are heritable...the damaged culture is passed along with its damage intact to the next generation.
• Note that the not using of antibiotics, and the incorporation of feral stock has allowed a much less damaged version of these communities to persist in Dee’s bees vs. the bees up the road.
• Antibiotic resistance is metabolically expensive. Populations that are selected for antibiotic resistance have less resources for functions other than antibiotic resistance…this is to say that antibiotic resistance comes at a cost to the population.
• If you don’t think small cost savings are important and affect evolution in relatively short time periods, note the isolated populations of cave fish. When eyes don’t do you any good, the rare genetic combinations/mutations that don’t develop eyes become dominant, simply because the energy not spent on eyes is spent in other ways that make those individuals more competitive.

 

 

Further supporting information is found in: Gut Microbes [yes, that is the journal name)] Functional and evolutionary insights into the simple yet specific gut microbiota of the honey bee from metagenomic analysis

Volume 4, Issue 1 January/February 2013
Keywords: Gilliamella, Snodgrassella, gut microbiome, insects, pectin, symbionts

Authors: Philipp Engel and Nancy A. Moran

From the abstract: "...Gene contents could be linked to different symbiotic functions with the host. Further, we found a high degree of genetic diversity within each of these species. In the case of the gammaproteobacterial species Gilliamella apicola, we could experimentally show a link between genetic variation of isolates and functional differences suggesting that niche partitioning within this species has emerged during evolution with its bee hosts."

- Dean