08.06.2015 Views

Vol. 51—1997 - NorthEastern Weed Science Society

Vol. 51—1997 - NorthEastern Weed Science Society

Vol. 51—1997 - NorthEastern Weed Science Society

SHOW MORE
SHOW LESS

You also want an ePaper? Increase the reach of your titles

YUMPU automatically turns print PDFs into web optimized ePapers that Google loves.

--------- +-<br />

I<br />

I<br />

I<br />

177<br />

Interact~ons Between Herbicide Use and Turfgrass Diseases<br />

I<br />

I<br />

Pee<br />

I<br />

Bruce Martin<br />

Plant Pathology and Physiology<br />

Clemson University<br />

Dee Research and Education Center<br />

Florence, SC<br />

Herbici4es are valuable tools for the maintenance of quality<br />

turfgrass st~nds. During development of herbicides, turfgrasses<br />

are screenedithoroughly for tolerance to the materials before<br />

labels are o*tained. Good tolerance to healthy stands of grasses<br />

for which th$ materials are labelled is usually obtained.<br />

However, occasionally, unforeseen or unusual stress conditions<br />

may lead to iurfgrass injury. Sometimes the stress can<br />

predispose t~e plant to greater susceptibility to pathogens, and<br />

sometimes th¢ herbicide adds to environmental stress or interacts<br />

with the host turfgrass plant to influence susceptibility to<br />

pathogens. i<br />

Herbicir'es and plant growth regulators don't always cause<br />

problems wit diseases. For example, some triazole fungicides,<br />

such as fena imol (RUBIGAN), have herbicidal and/or growth<br />

regulator chrracteristics as well as fungicidal activity. In the<br />

Southeasterni U.S., fenarimol is utilized as a preemergence<br />

herbicide fo~ Paa annua control as much as for its fungicidal<br />

properties. I_In other cases, herbicides or plant growth<br />

regulators a~fect nontarget organisms and may predispose<br />

turfgrasses ~o greater damage from pathogens, as well as inhibit<br />

the recoverY) of the turf after "active" disease has subsided.<br />

Some oiJ the affected non-target organisms may be stimulated<br />

or inhibited by herbicides. The effects can be direct or<br />

indirect, fqr instance, by influencing a pathogen's virulence<br />

through eff~cts on mycelial growth, spore germination, or<br />

sclerotium ~urvival (Altman and Campbell, Hodges). It is also<br />

possible th~t herbicides can act indirectly by modifying the<br />

relationship between the pathogen and certain antagonists, or the<br />

pathogen's ~nvironment. However, usually, documented effects<br />

have been iq the realm of "predisposition" where the host<br />

physiology ,nd susceptibility to pathogens is altered.<br />

There ~as not been much research in turf concerning<br />

herbicide-t~rfgrass disease interactions. However, Madison<br />

observed a $evere attack of brown patch in Kentucky bluegrass<br />

following afplication of 2,4,S-T and disodium methyl arsenate.<br />

Turgeon, et~al., reported increasing incidence of stripe smut of<br />

Kentucky bl~egrass following bandane application. Karr et. al.<br />

found in grfenhouse investigations that benefin and bensulide<br />

slightly inpreased severity of Rhizoctonia blight and dollar spot<br />

in bermudagrass and pythium blight on annual ryegrass. Other<br />

examples ari in the literature.<br />

It wasi observed in the turfgrass plots at Clemson<br />

II<br />

I<br />

I<br />

I<br />

I<br />

I<br />

II<br />

II<br />

I<br />

I

Hooray! Your file is uploaded and ready to be published.

Saved successfully!

Ooh no, something went wrong!