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From:
Charles Linder <[log in to unmask]>
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Informed Discussion of Beekeeping Issues and Bee Biology <[log in to unmask]>
Date:
Mon, 16 Oct 2017 08:29:46 -0500
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That was never the question--you're guilty of a "straw man" argument.  It is the prophylactic overuse of antibiotics that is the problem.


Not fair,  or correct,  You can't fairly use terms like "cherry picking" and "straw man"  just because you disagree.   One man's cherry picking is another mans gold nugget.  Throwing terms at the discussion in a personal form is.....???

  In this case there is a ton of evidence that says your wrong.  (see link below)    


Resistant strains have been and are everywhere Simple soil test show many of them,  current we know that penicillin resistant virus existed before penicillin.

>
>        >   I am 100% sure resistant strains will continue.....
>

Evidence is to the contrary, as resistance often incurs a cost to fitness.  

Not sure how you read that to come to that conclusion?  There are seemingly two forms of resistance,  acquired and preexistent.  One makes the case that this solves the issue,  but its quite obvious from the research there is zero chance of that.  Resistant forms already exist and mutate on their own.  While you can safely argue eliminating one strain leaves holes for the other to fill, you can't be claiming there all created by overuse?? Or that stopping some usage solves the problem??


(best information I have found on the topic below)

 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2937522/

For those who don't have time to read,  it’s a great compilation of information on resistance,  citing hundreds of strains  and highlighting what we know as well as what we don't know.  Bottom Line,  while many are sure "overuse" is the problem,  we actually don't know for sure.  Many "resistant" strains are already naturaling occurring and are simply unknown to us

Cloning, PCR, and gene expression techniques have been applied to detect natural r genes in random recombinant clones derived from bacterial DNA libraries from soils and sediments (3, 119). A potential problem is that the identification of functional resistance requires gene expression (transcription and translation) of the cloned genes in a heterologous host; to date, only E. coli has been used. Some r genes were identified, but one wonders how many would have been found using a wider range of expression systems and hosts; subsequent global sequencing approaches by D'Costa et al. (43) and Dantas et al. (36) indicate that the number would have been large. Taken together, these studies confirm the existence of many potential antibiotic r genes and mechanisms in nature.

Dantas and coworkers have taken a complementary approach to that of D'Costa et al. by screening soil bacteria for biochemical processes that degrade or inactivate antibiotics (36). Hundreds of strains were randomly isolated from 11 diverse urban and rural soils and tested for the ability to subsist or grow on one or more of 18 different antibiotics as sole carbon and nitrogen sources. Perhaps surprisingly, many strains were isolated that grew efficiently on common antimicrobials, including aminoglycosides, fluoroquinolones, and other classes. Most of the strains identified in this study were proteobacteria, and more than 40% were Burkholderia spp.; pseudomonads were also well represented. Obviously, catabolic pathways responsible for antibiotic digestion in nature provide a rich source of potential resistance determinants; additional studies should reveal novel mechanisms of resistance to most antibiotic classes. Work on antibiotic-catabolizing bacteria was reported in the 1970s (53), but the studies of Dantas and colleagues have exposed the full extent and distribution of degradation/r genes in the environment and further verified the roles played by reservoirs of soil bacteria as origins of antibiotic r genes.




We keep referring to propalactic treatment,  it’s a garbage term thrown about by those of us with no specific knowledge of the situation.  Many can quite correctly argue the majority of our mite treatments are propalactic in nature,  we know low viral loads can allow a fairly high level of mites,  and yet not a single one of us would ever make the claim to wait until DWV shows it head,  and yet we want to make claims and demand that of others?  Certain antibiotics in feeds shows clearly increased weight gains, more data than we have with fumigilan or Terra pro?  Seems to me the sublethal effects of contaminates in the feed supply were correctly addressed and documented.


Don't misread and think I disagree with the simple concept we may get by with less,  we very well may.  The problem is that regulations such as this are an idiotic (IMO) way to handle it.  Free market works fine,  and has for a long time.   Anitibiotic free chicken has become a marketing tool and a staple in 5 years.  This is a classic case of one group of people thinking they are smarter than the rest,  and need to force a point with fines and government backing, because they know the argument is weak. There are no winners here.  Just bullies and fees.







For our industry, one of the major honey packers has been making the point that US honey is no longer the "cleanest" honey in the world.  He's had to reject many loads due to antibiotic contamination.  All it is going to take is for an investigative report on this to go viral to really hurt the honey market.  Remember Alar?


The problem lies in the fact that only  a few are doing that testing.   And the culprits know and sell to smaller packing houses. I suspect  Like you do at some point there is going to be hell to pay.


Charles

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