Got a chance this week for a chat (AKA banter, debate, even argument) with my old pal Dan Dinelli. Anyone in this business with even the slightest interest in a broader environmental perspective on golf turf management knows Dan. I know him as a thoughtful, passionate steward of a piece of land (and exceptionally fine turf) that happens to be a great old country club on the north shore of Chicago. As usual our chat left me with more questions than answers.
The topic this time was Bacterial Etiolation (AKA mad tiller disease, etiolated tiller syndrome, etc.). Dan was in a lather! Concerned by the assertion that many have classified this issue as a secondary pathogen, Dan (and I) are old enough to remember when the last bacterial problem came through Chicago and virtually eliminated vegetatively propagated bentgrass greens, i.e., C-15 bentgrass decline. No one thought that problem was a secondary pathogen.
So here we are on a beautiful early summer morning with fresh dew still on the course actively being whipped and mowed, two Italian-Americans in a passionate discussion. Hoping an answer emerges, but as is often the case in my chats with Dan, the more I learn the less I know.
The ambiguity of the BE problem is vast. It strikes creeping bentgrass and annual bluegrass depending on the climate. It often strikes when humidity is high, but can be observed when temperatures are cool. There are at least two organisms, Acidovorax and Xanthomonas known to be involved, but others have been isolated. Dr. Paul Giordano conducted excellent and award winning research at Michigan State producing field symptoms and fulfilling Koch's Postulates (a series of four requirements that includes re-inoculating plants in the field and reproducing the symptoms).
Interestingly, some suggested the etiolation on bentgrass was worse when plugs or sod was brought in to a damaged area. Dr. Giordano used sodded bentgrass to produce his results, further supporting the notion that juvenility or hormonal issues might be involved since new plugs and sod often require significant hormone stimulus (cytokinins and auxins) to regenerate roots severed during the transplanting process.
Several band-wagons have started regarding what might cause predisposition to the problem. Often it is found on areas with a history of injury (anthracnose, winter kill). Often associated with juvenile plants attempting to recolonize an area. Some have suggested a hormonal association leading to a broad discussion about plant growth regulators and biostimulants. In fact, North Carolina State Ph.D. Candidate Joe Roberts has been involved in research investigating these claims (read more at: http://usgatero.msu.edu/v13/n2-19.pdf).
Sometimes Primo (trinexapac-ethyl) use increases the problem, sometimes it decreases. A few years ago there was some strong suspicion that biostimulants that might have hormonal properties such as humates and seaweed extracts could be involved. However in the preliminary work to date there was no association with these products and bacterial etiolation. Amid the cry to simply our management programs we should be careful, especially when allowing plants to release from growth regulation in the middle of summer!
A closer look at the PGR association reveals not all Gibberillic Acid (GA) Synthesis Blockers are created equal. Most agree that trinexapac a late-GA blocker, seems more involved than early GA-blockers flurprimidol and paclobutrazol. One could speculate that mode of action might be involved, but what about cytokinins and auxins?
Management of the problem has some confusion as well. Most agree oxytetracyclene (not currently labeled for use in turf) does halt the problem, but we want to be careful how far we wade into this approach, not just for legal issues but broader anti-biotic issues. Daconil Action and Signature have been touted as control options, yet others suggest a role for phosphites in exacerbating the problem.
As Dan and I wrapped up our two-hour banter, I'm not sure I assuaged his concern, but it certainly got us both thinking. More questions than answers once again and it seems the more I find out about this bacterial etiolation, the less I know.