Managing and preventingherbicideresistance in weeds

WRAG guidelines

2003

The Home-Grown Cereals Authority (HGCA) has provided funding for

some of the projects on which these guidelines are based but has not

conducted the research or written the guidelines.While the authors have

worked on the best information available to them, neither the HGCA nor

the authors shall in any event be liable for any loss, damage or injury

howsoever suffered directly or indirectly in relation to the guidelines or

the research on which they are based.

Reference herein to trade names and proprietary products without

stating that they are protected does not imply they may be regarded as

unprotected and thus free for general use. No endorsement of named

products is intended, nor is any criticism implied of other alternative, but

unnamed products.

If you are unsure about any of the suggested actions, orwant them interpreted for your local conditions, consult aprofessional agronomist.

Herbicide resistance is theinherited ability of a weed tosurvive a rate of herbicide thatwould normally kill it.

First identified in black-grass in1982, herbicide resistance also nowaffects wild-oats, Italian rye-grassand most recently commonchickweed and common poppy.

These guidelines bring together the latest research and fieldexperience.They aim to help UK farmers and advisers:

– prevent resistant weedpopulations developing

– manage existing resistantpopulations

– prevent the spread ofherbicide resistant weeds.

2

Background

Symptoms of resistance

◗ Healthy plants beside dead plantsof the same species.

◗ Poor control of one susceptiblespecies when other susceptiblespecies are well controlled.

◗ Discrete weed patches.

◗ Gradual decline in control overseveral years.

Years

Co

ntr

ol

The impact of herbicide resistance

Herbicide resistance typically increases production costsand limits options for herbicides, cultivations androtations. As weeds are relatively immobile, thedevelopment of resistance is usually due to practice onindividual farms.

How badly an individual farm is affected by herbicideresistance depends on which mechanism of resistancedevelops as well as the options for turning to alternativecrops and herbicides.

For instance, if target site resistance develops there maybe little immediate effect where alternative herbicides areavailable at a similar cost. However, increased reliance ona more limited range of modes of action increases therisk of further forms of resistance developing.

Production costs are most affected where the options foralternative cropping and herbicides are restricted. Forinstance, annual costs of herbicide resistance couldexceed £100/ha when the enhanced metabolism form ofresistance fully develops in black-grass within continuouswheat systems. Herbicide costs are likely to increase andyields may be more variable – and generally lower –because the start of drilling will have to be delayed. Inaddition, cultivation costs may also increase due to theneed for regular ploughing.

Annual costs can

exceed £100/ha

Backgro

un

d

3

Resistance testing

◗ Have a test carried out if you suspect resistance couldbe developing.The most commonly used tests are onweed seeds (see page 11).

◗ Collect samples, representative of the problem field orarea. Sample an area of about 100 m by 2-3 tramlines,unless the problem occurs in a smaller distinct patch.

◗ Collect samples of grassweed seeds in dryconditions during July.

• Gently rub headsover a bag so thatonly ripe seeds arecollected.

• Do not collect intact heads, as many seeds will beimmature.

• Allow seeds to dry in a shallow and opencontainer after collection.

• Store dried seeds in paper envelopes, notpolythene bags.

Results of seed testing can be obtained by

September for samples collected in July.

◗ Alternatively dig up at least 50 plants for each area tobe tested between autumn and early spring. Dispatchas soon as possible.

Results from plant samples can be obtained

within four weeks of dispatch.This may allow

improved herbicide decision-making within

the current season.

Herbicide resistance mechanisms

Herbicide resistance is an inherited trait. It occurs through the selection of plants able to survive herbicides.Withrepeated selection, resistant plants survive and multiply until they dominate the population.

The two main resistance mechanisms:

Enhanced metabolism

Enhanced metabolism results in herbicide detoxification.Resistance tends to be partial leading to poor weedcontrol. Plants may be cross-resistant to herbicides withdifferent modes of action. Currently, this is the mostcommon resistance mechanism in grass weeds in the UK.

Target site resistance

Target site resistance blocks the site of activity specific to the herbicide’s mode of action. This usually resultsin complete resistance to herbicides acting on thatspecific site but not to herbicides acting on differenttargets.Two types have been identified in the UK: oneaffects ‘fop’ and ‘dim’ grass weed herbicides (ACCaseinhibitors); the other affects sulfonylurea broad-leavedweed herbicides (ALS inhibitors). Resistant populationscan develop rapidly where target site resistance occurs,particularly if shallow cultivation is practised frequently.

The overall strategy

◗ Assess the resistance risk factorsfor your farm.

◗ Integrate cultural and chemicalcontrol in a long-term strategy.

◗ Minimise weed seed movementwithin and between fields.

◗ Monitor fields regularly and takeearly action to prevent patchesspreading.

◗ Manage the soil’s weed seedbank.

4

Principles

Cultural control

Use cultural control to reduce the need forherbicides and the risk of resistance developing.Many options are available, although some mayconflict with advice for control of pests anddiseases or for reducing nitrate leaching.

Plough to reduce resistance risk. It reduces weednumbers, particularly of species that are relatively non-persistent in the soil, eg black-grass and Italian rye-grass.It may also bring older, less selected seeds back to thesoil surface to increase the proportion of susceptibleplants in the weed population. Consider rotationalploughing every two to five years, if annual ploughing isnot feasible.

Use shallow non-plough tillage to avoid bringing largenumbers of weed seeds, ploughed down in the previousyear, to the surface.This is only appropriate where littleor no seed has been shed in the crop just harvested.

Consider mechanical weed control, eg harrowing.

Adopt as diverse a rotation as possible using autumnand spring-sown crops including non-cereals, to reducethe dominance of most annual grass weeds. Overallherbicide use may be reduced and the choice ofherbicide modes of action extended.

Use set-aside to reduce weed populations by preventingseeding.

Delay drilling winter cereals to allow a highproportion of weed seedlings to emerge and becontrolled before sowing. Black-grass and Italian rye-grassinfestations can be effectively reduced if there issufficient soil moisture for germination. Badly infestedfields should be sown last.

Spray stubble or seedbeds with a non-selectiveherbicide to ensure that all weed seedlings which haveemerged before sowing are destroyed.

Establish competitive crops using appropriate seedrates, more competitive varieties or narrower rows inorder to suppress weeds.

Prevent seed return by cutting or spraying off weedpatches with a non-selective herbicide. Hand roguing isfeasible at low weed populations or for patches of tallweeds, eg wild-oats.

Avoid spreading resistant seeds and plants.This canoccur through contaminated seed, combine harvesters,cultivation equipment, straw or manure. All fieldequipment and clothing should be cleaned betweenfields.

Weeds are relatively immobile compared to diseases orpests. Herbicide resistance usually develops on individualfarms due to the weed control programmes used.

Herbicide resistance can be more easily prevented on aspecific farm, compared to fungicide or insecticideresistance.

Occurrence

of resistance

is usually due

to practice on

individual farms

Herbicide control

◗ Use tank/product mixes or sequences of herbicideswith different modes of action within individualcrops, or successive crops (see page 10).

◗ When using a tank/product mix, or sequence, ensurethat two or more components with different modes ofaction are active against the target weeds, especiallythose that have developed resistance in the UK.

◗ Do not rely on ‘fops’ and ‘dims’ or the ALS inhibitors,eg sulfonylureas, as the sole means of grass weedcontrol in consecutive crops.The risk of rapiddevelopment of target site resistance is high.

◗ Treat weeds when small and actively growing tomaximise control of resistant weeds.

Monitoring

◗ Keep accurate field records. Record details ofcropping, cultivations, herbicide use (including modeof action) and control achieved.

◗ Monitor herbicide performance.

◗ Be aware of resistance developing in the locality.

◗ Test specific fields – either those with a knowndegree of resistance or where there is a high risk ofresistance developing – every three years.This willprovide a measure of the success of the resistancemanagement strategy.

Prin

ciples

5

Cropping system Good rotation of spring and autumn crops Continuous winter cereals

Cultivation system Annual ploughing Continuous non-ploughing

Control method Cultural only Herbicides only

Herbicide use throughout Different modes of action Single mode of action the rotation

Weed infestation level Low High

Resistance incidence None in vicinity Identified locally in similar cropping systems

Agronomic factor Lowest risk Highest risk

Herbicide resistance risk factors

Herbicide resistance can threaten the sustainability of arable cropping – take action early to minimise the risk.

With resistance widespread there needs to be agreater reliance on cultural control measures,particularly crop rotation, ploughing and time ofdrilling. Farmers should monitor regularly thedegree of resistance to ensure that current policiesare not causing a further increase.

Enhanced metabolism resistance is widespread andreduces the performance of most of the effective cerealherbicides but the extent of cross-resistance varies.Herbicides little or unaffected by this mechanism includetrifluralin, flufenacet, tri-allate, propyzamide, carbetamide,ethofumesate, metazachlor and the ‘dims’ – cycloxydimand tepraloxydim. Many can only be used in non-cerealcrops, highlighting the importance of crop rotation.

The incidence of target site resistance to ‘fops’ and ‘dims’is steadily increasing.There is concern that target siteresistance to ALS inhibitors, used against grass weeds,could occur as has already happened in broad-leavedweeds.To avoid, or delay, resistance developing, neither‘fops’ and ‘dims’ nor ALS-inhibiting herbicides should berelied on as the sole means of black-grass control insuccessive crops.

6

Black-grassAlopecurus myosuroides

Black-grass

Resistant black-grass

Resistance status Enhanced metabolism – widespread Target site resistance to ‘fops’ and ‘dims’ – increasing threatTarget site resistance to ALS inhibitors – potential threat

Confirmed cases of herbicide resistance in the UK – 2002

First found 1982

Cases confirmed Over 1000

Number of counties 30

◗ Monitor regularly, eg every three years, the degree of resistance in specific fields to assess success of theresistance management strategy adopted.

◗ Take early action against any identified patches.

◗ Place more reliance on cultural control measures, egploughing and spring cropping.

◗ Minimise weed seed movement within and betweenfields.

◗ Drill heavily infested fields at the end of the autumnprogramme.

◗ In winter cereals include a pre-emergence herbicide,eg trifluralin, tri-allate or flufenacet + pendimethalin, ina sequence to improve control of resistantpopulations.

◗ Apply post-emergence herbicides to small and activelygrowing weeds to maximise control.

◗ Do not use ‘fops’, ‘dims’ or ALS inhibitors as the solemeans of grass weed control in consecutive crops dueto the risk of rapid development of target siteresistance.

◗ Investigate why individual black-grass plants surviveunscathed from applications of a ‘fop’, ‘dim’ or an ALS-inhibiting black-grass herbicide.These may havetarget site resistance.

◗ Use herbicides with different modes of action in tankmixes or sequences to reduce the risk of resistancedeveloping.

◗ Ensure that at least two components of tank mixes orsequences are active against black-grass.

Action:

◗ Where possible avoid sowing Italian rye-grass on arable farms.

◗ Minimise weed seed movement within and between fields.

◗ Hand rogue initial low level infestations to preventpatches spreading across fields.

◗ Plough to bury seed effectively.

◗ Consider spring cropping to reduce weed pressure ordrill contaminated fields last in the autumn programme.

◗ When using a tank/product mix, or sequence, ensurethat two or more components, with different modes of action are active against Italian rye-grass.

◗ Do not use ‘fops’, ‘dims’ or ALS inhibitors as the solemeans of grass weed control in consecutive crops dueto the risk of target site resistance.

◗ Investigate why individual plants survive an applicationof a ‘fop’, ‘dim’ or an ALS-inhibiting herbicide unscathed.

◗ Where resistance to ‘fops’ or ‘dims’ occurs, do not applyany herbicides with this mode of action to that field.

◗ Where resistance occurs in winter cereals, use asequence of pre-emergence herbicide, eg flufenacet +pendimethalin or tri-allate, followed by an early post-emergence application of chlorotoluron (check varietytolerance) or a product containing flurtamone.

◗ Apply post-emergence herbicides to small, activelygrowing weeds to maximise control.

◗ Consider non-cereals for a wider herbicide choice, eg:• cycloxydim and tepraloxydim (unaffected by

enhanced metabolism),• propyzamide, carbetamide, metazachlor or

trifluralin (appear unaffected by either mechanism).

◗ Monitor regularly, eg every three years, the degree ofresistance in specific fields to assess success of theresistance management strategy adopted.

Italian rye-grass

7

Herbicide resistance is rapidly increasing in someareas. The main emphasis must be on culturaloptions – rotation, cultivation and preventing weedspread – to both control resistant populations andprevent resistance developing.

Italian rye-grass is very prolific. It often grows as a weedon farms where it has not been sown and can occur onall-arable farms. It can cause substantial yield losses.

Populations have evolved both enhanced metabolism andtarget site resistance to the ‘fop’ and ‘dim’ herbicides.

The enhanced metabolism mechanism of resistance cansubstantially reduce the efficacy of ‘fop’ and some ‘dim’herbicides such as diclofop-methyl and tralkoxydim.Herbicides whose performance is little or unaffected bythis mechanism include flufenacet + pendimethalin, tri-allate, chlorotoluron and flurtamone.

Target site resistance, currently much less common, islikely to increase.

Herbicide-resistant perennial rye-grass (Lolium perenne)occurs much less frequently.

Action:

Italian rye-grassLolium multiflorum

Resistance status Enhanced metabolism – increasingly commonTarget site resistance – increasing threat

ResistantItalianrye-grass

Confirmed cases of herbicide resistance in the UK – 2002

First found 1990

Cases confirmed Over 100

Number of counties 21

For most farms there should be a preventativepolicy, based on herbicide rotation, to stopresistance occurring. The success of this strategyshould be regularly monitored.

Resistance occurs in both common and winterwild-oats. Changes in cultivation or drilling date dolittle to reduce emergence of common wild-oats.However, many instances of resistance are inwinter wild-oat populations, which springcropping will reduce.

Enhanced metabolism results in partial resistance to the‘fops’ and also cross-resistance to the ‘dim’ tralkoxydim,and to other herbicides, eg imazamethabenz-methyl andflamprop-M-isopropyl.

Some wild-oat populations have target site resistance.However, these are only resistant to ‘fops’, not ‘dims’ orany other herbicides.

To date, no resistance has been found to tri-allate,isoproturon (IPU), difenzoquat, tepraloxydim orcycloxydim in the UK.

◗ Rotate herbicide modes of action.

◗ Rotate crops to:

• allow a greater range of herbicide modes of actionto be used,

• reduce populations of winter wild-oats.

◗ Map wild-oat patches and do not assume they arespray ‘misses’. Act early to prevent patches spreadingacross fields.

◗ Hand rogue intensively or spray patches with non-selective weedkillers to prevent spread.

◗ Reduce reliance on ‘fops’ and ‘dims’ by using herbicides with alternative modes of action.

◗ Delay cultivation for as long as possible after harvest,ideally over winter, to allow birds and mammals timeto eat seeds shed from the previous crop.

◗ Minimise weed seed movement in combines, straw,cultivation equipment and by other means.

◗ Monitor herbicide performance and identify causes ofpoor activity.

◗ Test seed if resistance is suspected.

◗ Apply post-emergence herbicides when weeds aresmall (1-3 leaves) to maximise control of partiallyresistant wild-oats. Plants with target site resistance are unlikely to be controlled by the ‘fops’ at any timing.

Action:

8

Co

mm

on and w

inter wild-o

ats

Resistance status Widely distributed but infrequent

Wild-oats common wild-oats winter wild-oats Avena fatua Avena sterilis ssp. ludoviciana

Resistantwild-oats

Confirmed cases of herbicide resistance in the UK – 2002

First found 1993

Cases confirmed Under 100

Number of counties 21

Common chickweed plants resistant tosulfonylurea herbicides were first identifiedin Scotland in one field in 2000.Thatpopulation had target site resistance.Sulfonylurea-resistant chickweed wasconfirmed on a further five farms in 2001.Most samples came from Scotland.Twosamples came from intensive winter cerealrotations in south and east England.

One sulfonylurea-resistant chickweed population, in Scotland, showedcross-resistance to florasulam – a triazolopyrimidine.

◗ Rotate herbicides with different modes of action or use mixtures.

◗ Do not rely solely on one mode of action, eg ALS inhibitors, in the same field over several years.

◗ Investigate odd patches of unexplained poor control of any broad-leaved weed, particularly in long runs of cerealswhere ALS inhibitors have been the main herbicides used for broad-leaved weed control.

◗ Treat weeds which are small and actively growing for maximum control.

Bro

ad-leaved weeds

9

Action:

Common chickweed Stellaria media

Broad-leaved weedsCurrently very few instances of herbicide resistance in broad-leaved weeds occur in the UK. The emphasisshould be on preventing resistance through rotating herbicide modes of action and/or using effectiveherbicide mixtures. Crop rotations allow the use of a wide range of herbicide modes of action.

Recently, some broad-leaved weeds have been found to be resistant to ALS-inhibiting herbicides in the UK.

Resistance Limited, first found in 2000status

Common poppyplants, resistant tosulfonylureaherbicides, werefound on three farmsin south and eastEngland in 2001.Allcame from fieldsunder intensivewinter cerealrotations.

Common poppy Papaver rhoeas

Resistance Limited, first found status in 2001

The five groups of ALS-inhibiting herbicides

Worldwide, resistanceto the ALS mode ofaction continues toincrease. Cross-resistance patternsbetween groups thatinhibit ALS arecomplex and difficultto predict.

chickweed bromoxynil + ioxynil, chlorotoluron,diflufenican, fluroxypyr, isoproturon,mecoprop, pendimethalin

poppy bromoxynil + ioxynil, chlorotoluron,isoproturon, MCPA, pendimethalin

Weed Herbicide

Some effective non ALS-inhibiting cereal herbicidesConfirmed cases of herbicide resistance in the UK – 2002

Common Commonchickweed poppy

First found 2000 2001

Cases confirmed 6 3

Number of counties 2 Scotland 3 England2 England

sulfonylureas metsulfuron, flupyrsulfuron, sulfosulfuron, amidosulfuron,tribenuron, thifensulfuron, iodosulfuron

triazolopyrimidines florasulam

imidazolinones imazamethabenz

sulfonylaminocarbonyltriazolinones propoxycarbazone-sodium

pyrimidinylthiobenzoates none in UK

Group Examples

Group Mode of action Chemical Family Active Product nameIngredient (example)

A Inhibition of acetyl Aryloxyphenoxy- clodinafop-propargyl TopikCoA carboxylase propionates diclofop-methyl in Tigress Ultra(ACCase inhibitors) (‘fops’) fenoxaprop-P-ethyl Cheetah Super

fluazifop-P-butyl Fusiladepropaquizafop Falconquizalofop-P-ethyl Sceptre

Cyclohexanediones cycloxydim Laser(‘dims’) sethoxydim Checkmate

tepraloxydim Aramotralkoxydim Grasp

B Inhibition of acetolactate Sulfonylureas flupyrsulfuron-methyl Lexussynthase (ALS inhibitors) sulfosulfuron Monitor

Sulfonylaminocarbonyl propoxycarbazone-Na Attribut-triazolinones

Imidazolinones imazamethabenz-methyl Dagger

C1 Inhibition of Triazines atrazine variousphotosynthesis at cyanazine Fortrolphotosystem II simazine various

terbutryn Alpha Terbutryn

Triazinones metribuzin Sencorex

C2 Inhibition of Ureas chlorotoluron variousphotosynthesis at isoproturon variousphotosystem II methabenzthiazuron Tribunil

metoxuron Dosaflo

D Photosystem 1 Bipyridyliums paraquat Gramoxone– electron diversion

F1 Inhibition of pigment Inhibitors of PDS flurtamone in Bacarasynthesis (bleaching)

F3 Inhibition of pigment Unknown target amitrole Weedazolsynthesis (bleaching)

G Inhibition of EPSP Glycines glyphosate Roundupsynthase

H Inhibition of Phosphinic acids glufosinate-ammonium Challengeglutamine synthetase

K1 Inhibition of microtubule Benzamides propyzamide Kerbassembly tebutam Comodor

Dinitroaniline pendimethalin Stomptrifluralin Treflan

K2 Inhibition of microtubule Carbamates carbetamide Carbetamexorganisation propham Tripart Sentinel

K3 Inhibition of Acetamides napropamide Devrinol cell division

Chloroacetamides metazachlor Butisan

Oxyacetamides flufenacet in Crystal

N Inhibition of lipid Thiocarbamates tri-allate Avadexsynthesis – not

Benzofuranes ethofumesate NortronACCase inhibition

Z Unknown – flamprop-M-isopropyl Commandodifenzoquat Avenge

Group Mode of action Chemical family Active Product nameingredient (example)

10

Herbicides for control of black-grass, wild-oats or Italian rye-grass grouped according tobiochemical mode of action

This table is based on information in “The UK Pesticide Guide 2002”, Editor: R.Whitehead, CAB International/British Crop Protection Council, and “The World ofHerbicides according to HRAC classification on mode of action 2002” document, produced by the Herbicide Resistance Action Committee (HRAC).

Further reading and contacts

Further reading and co

n

HGCA publications

Topic Sheet 22 (1999) – Preventing and controllingherbicide-resistant grass weeds (free)

Topic Sheet 46 (2001) – Dealing with herbicide-resistant wild-oats (free)

Project Report 116 (1995) – Inheritance of herbicideresistance in black-grass (Alopecurus myosuroides) andresponses of the weed to a range of herbicides

Project Report 131 (1996) – Effects of soil type,weather and resistance on efficacy of herbicides againstblack-grass

Project Report 225 (2000) – Towards a diagnostic testfor herbicide resistance in grasses

Project Report 266 (2001) – Developing strategies forreducing the risk from herbicide-resistant wild-oats

Project Report 279 (2002) – Detection of herbicideresistance in black-grass, Italian rye-grass and wild-oatsat all growth stages

tacts

Resistance testing

Contact your consultant, adviser or agrochemicalsupplier for availability of seed or plant tests.

Organisations offering resistance testing include:

Defra reports*

PT0208 (1996) – Genetic variation in resistance toherbicides – variability in herbicide performance

PT0209 (1997) – Susceptibility of arable weeds toherbicides

PT0211 (2001) – Developing strategies for reducingthe risk from herbicide-resistant wild-oats

PT0217/8 (2000) – Herbicide resistance in black-grassand wild-oats

*Available via e-mail from arable@defra.gsi.gov.uk

Other publications

Rothamsted Rapid Resistance Test for detectingherbicide resistance in black-grass, wild-oats andItalian rye-grass (1999).Written by Stephen Moss.Rothamsted Research Technical Booklet, 16 pages

The UK Pesticide Guide 2003. Edited by R Whitehead.Published by CAB International/British Crop ProtectionCouncil

The World of Herbicides according to the HRACclassification on mode of action 2002. Published bythe Herbicide Resistance Action Committee

Weed Management Handbook, 9th edition (2002).Edited by R E L Naylor. Published for the British CropProtection Council by Blackwell Science Ltd., Oxford.423 pages

Web sites

Defra: www.defra.gov.uk

HGCA: www.hgca.com

Herbicide Resistance Action Committee (HRAC):www.plantprotection.org/HRAC/

Weed Resistance Action Group (WRAG):www.pesticides.gov.uk/committees/resistance/index.htm

Worldwide Herbicide Resistance Information:www.weedscience.com

11

ADAS Boxworth (Tel: 01954 267666)

Oxford Plant Sciences (Tel: 01869 243333)

For information on HGCA services, pleasecontact the appropriate department.

Research and DevelopmentTel: 020 7520 3945E-mail: research@hgca.com

PublicationsTel: 020 7520 3920Fax: 020 7520 3931E-mail: publications@hgca.com

Website: www.hgca.com

HGCA, Caledonia House,223 Pentonville Road, London N1 9HJ

Acknowledgments

These guidelines were prepared by Dr Stephen Moss

(Rothamsted Research and Secretary of WRAG) and Jim Orson

(Morley Research Centre and Chairman of WRAG) with advice

from the WRAG committee – Dr Gordon Anderson-Taylor

(Bayer CropScience), James Clarke (ADAS Boxworth), Steve

Cranwell (Du Pont), Brin Hughes (UAP), Chris Rundle (PSD)

and Dr Pat Ryan (Syngenta).

WRAG gratefully acknowledges Defra and HGCA for funding

much of the research into herbicide resistance and HGCA for

funding this publication.

Edited by Dr Clive Edwards, HGCA and Geoff Dodgson,

Chamberlain.

Design by Chamberlain.

The Weed Resistance Action Group (WRAG) was formed in

1989 and comprises an informal group of representatives from

Crop Protection Association (CPA) member companies,

distributors and independent organisations involved in

herbicide resistance research in the UK.

© HGCA 2003

(free to HGCA levy payers)