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Herbicide-resistant weed biotypes will become increasingly prevalent in plantations where herbicides are used routinely.
Resistant biotypes are often less vigorous or fit than susceptible biotypes where no herbicides are used. Where herbicides are applied, particularly those that persist in the soil, susceptible biotypes are killed and the less fit resistant ones build up rapidly in the absence of competition.
The development of resistant biotypes could be retarded by easing the selection pressure through reducing the use of herbicides. The more vigorous, susceptible biotypes would then suppress the less fit resistant ones. However few growers in Western Europe could return to a situation where weeds are controlled by cultivation alone.
Rotation delays the development of resistance. With perennial fruits, where crop rotation is impossible, rotation of herbicides is imperative using chemicals with different mechanisms of action.
Where some hand labour is available to supplement the use of herbicides, the development of resistant biotypes could be prevented by a policy of zero tolerance for weeds, i.e. by killing weeds before they are able to reproduce themselves.
Resistant weeds increase management costs. Although expensive in the short term, a policy of zero tolerance for weeds could well be economic in some situations if assessed over a period of years.
The widespread development of weed biotypes with resistance to triazine and other herbicides is a major threat to fruit growers. Simazine, in particular, is recommended for use in a range of fruit crops (Fryer and Makepeace, 1978). The efficacy of this herbicide is due to its high phytotoxicity, wide weed spectrum and relatively long persistance in the soil. These same factors also tend to maximise effective kill of weeds. This increases the selection pressure and hence encourages the development of resistant biotypes (Murphy, 1983).
Compared with insects and plant pathogens, resistance in weeds developed slowly. Although the first record of the development of pesticide resistance in insects occurred in 1908 (Melander, 1914), nearly half a century passed before similar problems occurred with herbicides. Harpur (1956) warned that it was only a matter of time before presently susceptible weeds would acquire resistance to herbicides. Despite his warning the threat of resistant weeds was generally ignored by scientists and growers.
This complacency and the long delay in the occurrence of herbicide-resistant biotypes was due to a number of factors. Compared with other pesticides, relatively small amounts of herbicides were used until the 1950s and 60s. In addition, few weeds produce more than one generation a year and they are less mobile than insects and fungal diseases (LeBaron and Gressel, 1982).
The first records of acquired resistance in weeds related to the herbicide 2,4-D and began to appear around the mid 1950s. McCall (1954) reported that Commelina diffusa and other weeds were becoming more difficult to control in sugar cane plantations in Hawaii. Pfeiffer (1956) reported that seed obtained from weeds surviving 2,4-D treatment produced plants about twice as resistant as the previous generation.
Although Ryan (1970) first reported the development of simazine resistance in Senecio vulgaris in North America during the 1960s, the problem only emerged in Europe in the late 1970s. Within a few years many reports of simazine-resistant biotypes appeared in a number of countries. Simazine-resistant biotypes were first recorded in France in 1978 (Gasquez and Darmency, 1979), the UK in 1980 (Putwain, 1982), Belgium in 1981 (Bulcke et al, 1984) and the Netherlands mainly between 1985 and 1987 (van Oorschot, 1989).
Since the early 1980s triazine resistance has developed in most countries where these herbicides have been used, extending from North America, through western and eastern Europe (Sovljanski et al, 1989) to Japan. In France alone, resistant biotypes are spreading on thousands of hectares of vineyards and on more than 500,000 ha of maize (Gasquez and Darmency, 1989).
Weed species with acquired resistance
In a number of countries, Senecio vulgaris was the first species to show resistance to simazine (Ryan, 1970: Clay and Underwood, 1989). During the late 1970s and early 1980s similar resistance occurred in many other species. For example, in the UK, Poa annua (Putwain, 1982), Epilobium ciliatum (Bailey et al, 1982), Erigeron canadense (Clay and West, 1987) and Chamomilla suaveolens (Clay, 1987) now show resistance to simazine.
In the Netherlands, chloroplastic resistance to triazines has been observed on 11 weed species, most of the findings being made between 1985 and 1987 (van Oorschot, 1989). In addition to the first three species listed above, these were Chenopodium album, C. ficifolium, Galinsoga ciliatum, Polygonum lapathifolium, P.aviculare, P. convolvulus, P. persicaria and Solanum nigrum. In Belgium, the most important triazine-resistant species is Echinocloa crus-galli (Bulcke and van Himme, 1989). In France triazine-resistant biotypes of 21 dicot and grass weed species have been recorded between 1978 and 1981 (Gasquez and Darmency, 1989). World wide over 50 species have now developed resistance to simazine/atrazine. Most of these weeds are annuals which produce large quantities of seed, thereby increasing the possibilities of genetic change and the development of resistance.
Although resistant biotypes were recorded first with phenoxyacetic acid type herbicides and are now most generally associated with triazines, resistance to other herbicide groups is also reported. In the UK, resistance to paraquat has been found in two species, Poa annua (Putwain, 1982) and Epilobium ciliatum (Clay, 1987). Chlorotoluron-resistant Alopecurus myosuroides has been recorded in England (Moss and Kemp, 1989) and glyphosate-resistant Convolvulus arvensis in Denmark (Haas and Streibig, 1989).
Cause of resistance
Weeds are excellent strategists and are ready to adapt to any change in control measures used against them. The store of weed seeds in the soil is enormous; there can be 375 to 750 million seeds/ha in arable land (Radosevich and Holt, 1984). In addition, within the seeds of any one species there are differences in genetic make-up. This genetic variability and the large seed reserve enable weeds to adapt to changing environments and so survive.
Because of widespread genetic variability, a small number of resistant individuals occur naturally in many species within a particular weed population (Conrad and Radosevich, 1982). Resistant biotypes tend to be less vigorous or fit than susceptible biotypes in situations where no herbicides are applied. Where cultivations are used to control weeds, both biotypes are suppressed and numbers of the potentially resistant biotypes are kept particularly low, because of their lower level of fitness. When herbicides are introduced, particularly those that persist in the soil, susceptible biotypes are killed and the less fit, resistant ones are enabled to grow and shed large quantities of seed because they have no competition (Gressel and Segel, 1982). When a herbicide is used repeatedly, long-term suppression of the normal weed population - the susceptible types - is achieved but resistant types gradually build up. Consequently resistance occurs most frequently where a single herbicide is used repeatedly on the same land for a number of years, as in fruit plantations.
Although paraquat has no residual effect, resistance has developed in a number of areas where this herbicide has been applied frequently each year for a number of years.
Physiological basis of resistance
Haas and Streibig (1989) have discussed the mechanisms used by weeds to acquire herbicide tolerance. These include:-
- changes in the way the weed absorbs, translocates or compartmentalises the herbicide.
- the weed may break down the herbicide into harmless components.
- the weed may be able to produce more of the enzyme that is being inhibited by the herbicide.
- there may be a small change in the site of action of the herbicide within the weed plant.
This last method is responsible for resistance to simazine and other triazines in a number of species. In susceptible weeds, simazine binds with the chloroplasts in the leaf cells and prevents the plants from photosynthesising. In resistant biotypes a small alteration in the binding site for triazines by way of interchanging one amino acid prevents any affinity of triazines to the binding site (Haas and Streibig, 1989). Consequently applied triazines have little if any effect on photosynthesis.
In Denmark, Convolvulus arvensis has developed resistance to glyphosate. In susceptible plants, glyphosate inhibits EPSP-synthease, a key enzyme responsible for the production of proteins essential for plant growth. Haas and Streibig (1989) suggest that resistant Convolvulus is able to produce an excess of EPSP-synthease compared with susceptible biotypes and in this way can tolerate higher concentrations of glyphosate.
Identification of resistant biotypes.
The early identification of resistant biotypes is important for a number of reasons. Early warning of the build-up of resistant species promotes the use of alternative herbicides. Thus, the high cost to growers and the environment, resulting from the use of ineffective herbicides, is avoided and the spread of resistant weeds is minimised. Methods of identifying resistant populations have been developed by Clay and Underwood (1989). These include standard dose-response pot tests and a leaf disc flotation technique, which gives a result on triazine resistance within two hours. Clay's results show that resistant biotypes may be unaffected by pre-emergence doses of simazine up to 1,000 times those lethal to the susceptible type.
Control of resistant weeds
In short-term crops an important measure against the development of resistant biotypes is rotation. As would be expected, resistance occurs most readily in perennial crops where rotation is impossible and in annual crops where monoculture or a narrow crop rotation has been practised (Bulcke and van Himme, 1989).
In crop situations where rotation cannot be adopted, the obvious way to tackle the problem of resistance is to rotate herbicides. However, it is not enough to change from one herbicide to another. The new herbicide must have a different mechanism of action on the weed or cross resistance could develop quickly. For example, Rubow (1989) suggests that, where Erigeron canadense has become resistant to triazines, clopyralid would be preferable to hexazinone as this latter herbicide is also in the triazine group. Even if a substitute herbicide can be found with a different method of action, resistance could also develop in time.
At present, triazine-resistant Senecio vulgaris and many other species can be controlled by napropamide, linuron, diuron and dichlobenil. Poa annua can be controlled by early propyzamide application either in a mixture with, or followed by, diuron (Bulcke and van Himme, 1989). Other herbicides showing promise in Belgium against resistant biotypes are metazachlor, chlorotoluron, methabenzthiazuron and isoxaben (van Himme, 1988). Bulcke and van Himme (1989) also report satisfactory control of simazine-resistant Poa annua in late winter with propyzamide or glyphosate and during the growing season with the graminicide haloxyfop-ethoxyethyl.
Easing the selection pressure
Arising mainly from fears of a build- up of chemical residues in ground water, many European scientists believe that the use of herbicides should be reduced and lower standards of weed control accepted (El Titi, 1989). In addition, because resistant biotypes tend to be less fit than susceptible ones, removing the herbicide will ease the selection pressure on a mixed population of resistant and susceptible biotypes. The more vigorous, susceptible type will gradually suppress the resistant type and the proportion of resistant types will decrease rapidly (Haas and Streibig, 1989). However high labour costs make it unlikely that many fruit growers in north west Europe could return to a situation where weeds were controlled by cultivation alone. Also, in intensively grown horticultural crops, where high yields are essential, it would be impracticable to suppress resistant biotypes by allowing the development of high populations of more vigorous susceptible types.
A policy of zero tolerance for weeds?
The only certain means of preventing the build-up of resistant biotypes is to prevent weeds from propagating themselves (either by seed or vegetatively) by the adoption of a policy of zero tolerance for weeds.
Where simazine is applied to clean, moist soil, weeds may survive for varied reasons. They may be perennial and have large underground food reserves (such as Elymus repens), or inherently tolerant (such as Galium aparine) or they may be a resistant type of a normally susceptible species (such as Senecio vulgaris). If perennial weeds are eliminated before planting the fruit crop and if large populations of weeds with acquired resistance have not yet developed, simazine can still give a very high standard of weed control in many areas.
When simazine was introduced in the late 1950s and early 60s many growers achieved almost complete weed control. In the absence of resistant biotypes, their crops grew in an almost weed-free environment for part of the year at least. The few widely scattered weeds that survived in these situations did not cause any loss of yield. Understandably, but unfortunately, they were ignored by fruit growers as it was uneconomic to control them, when judged solely on the basis of short-term economics. Hence the problem of resistant biotypes.
If it were possible, either by the use of alternative chemicals or physical means, to control the small numbers of weeds that survive a simazine application in a situation where resistant biotypes are not yet widespread, (and so prevent the build-up of resistance), this could change significantly the economics of crop production. A policy of zero tolerance for weeds would increase the cost of weed control in the short term, but could well prove economic if assessed over a period of years.
The possibility of achieving complete control of weeds, over a long-term period, was tested in a 1.5 ha amenity area (Robinson, 1989). Almost complete control of weeds was obtained with two applications of simazine or atrazine each year supplemented by spot-treatment of surviving weeds (largely with glyphosate) and a small amount of hand weeding. Although it was not possible to achieve complete weed control, the amount of seed shedding was reduced to a low level. So far resistant biotypes have not developed after repeated application of simazine or atrazine for 20 years.
The results suggest that, in areas where resistant biotypes have not yet developed, fruit growers could, at least, extend considerably the effective life of soil-acting herbicides. This could be achieved if growers were made aware of the threat of resistant biotypes and made greater efforts to prevent weeds shedding seeds by the use of chemical and physical control measures.
So far relatively few weed species have developed resistance. But with the versatility and adaptability of weeds and the range of mechanisms that they can use to escape the effects of herbicides, it is inevitable that resistance will continue to build up in large numbers of species. Within a few years the problem will be much worse.
Achieving a high standard of weed control so that no seed shedding occurs, requires great management skills and many growers would find it an impossible target. The versatility and adaptability of weeds make it impossible to control weeds solely by chemical means. However the rapid spread of herbicide-resistant weeds suggests that, in intensively grown crops, a more aggressive approach to weed control, using both chemical and physical methods, would be justified.
A policy of zero-tolerance for weeds could only be adopted in high value perennial crops, which would stand the cost of sequential herbicide and cultural treatments and which could tolerate broad-spectrum, soil-acting herbicides such as napropamide or simazine.
Preventing weeds from seeding need not involve the use of large quantities of herbicide. Much can be done by good management to reduce the amount of chemicals used. Herbicides used against emerged weeds should normally be applied as spot treatments using optimum amounts of water to minimise or avoid run-off onto the soil. In some situations, e.g. where light stands of Senecio vulgaris occur, hand pulling and removal would be possible.
- Bailey, J.A., Richardson, W.G., and Jones, A.G., 1982. The response of willow herbs (Epilobium adenocaulon and E. obscurum) to pre- or post-emergence herbicides. Proc. 1982 British Crop Protection Conference - Weeds:229-305.
- Bulcke, R., De Praeter, H., van Himme, M. and Stryckers, J., 1984 Resistance of annual meadow grass, Poa annua L., to 2-chloro-1,3,5-triazines. Med. Fac. Landbouww. Rijksun. Gent, 49(3b):1041-1050
- Bulcke, R., and van Himme, M., 1989. Resistance to herbicides in weeds in Belgium. CEC. Proc. of Meeting of EC Experts' Group, Tollose, Denmark, 1988. (In press).
- Clay, D.V., 1987. The response of simazine-resistant and susceptible biotypes of Chamomilla suaveolens, Epilobium ciliatum and Senecio vulgaris to other herbicides. Proc. 1987 British Crop Protection Conference - Weeds: 925-932.
- Clay, D.V. and Underwood, C., 1989. The identification of triazine- and paraquat-resistant weed biotypes and their response to other herbicides. CEC. Proc. of Meeting of EC Experts' Group, Tollose, Denmark, 1988. (In press).
- Clay, D. V., and West, T.M., 1987. The response of triazine- resistant and susceptible biotypes of Erigeron canadense to 23 herbicides. Med. Fac. Landbouww. Rijksuniv. Gent, 52(3b):1195- 1205.
- Conrad, S.G. and Radosevich, S.R., 1982. Ecological fitness of Senecio vulgaris and Amaranthus retroflexus biotypes susceptible or resistant to atrazine. J. Appl. Ecol., 16:171-177.
- El Titi, A., 1989. Personal communication.
- Fryer, J.D. and Makepeace, R.J., 1978. Weed Control Handbook. 8th Edition, Vol 2. Recommendations. Blackwell Scientific Publications, Oxford:136-155.
- Gasquez, J. and Darmency, H., 1989. Herbicide resistance in France. CEC. Proc. of Meeting of EC Experts' Group, Tollose, Denmark, 1988. (In press).
- Gressel, J. and Segel, L.A. 1982. Interrelating factors controlling the rate of appearance of resistance. In: LeBaron H.M. and Gressel, J.(Eds). Herbicide Resistance in Plants. Wiley and Sons, New York:325-337.
- Haas, H. and Streibig, J.C.,1989. Herbicide resistant weeds - threat or challenge? CEC. Proc. of Meeting of EC Experts' Group, Tollose, Denmark, 1988. (In Press).
- Harpur, J. L., 1956. The evolution of weeds in relation to their resistance to herbicides. Proc. Third British Weed Control Conference. 1956, 1:179-188.
- LeBaron, H.M. and Gressel, J., 1982. Summary of accomplishments, conclusions and future needs. In: LeBaron, H.M. and Gressel J.(Eds). Herbicide Resistance in Plants. Wiley and Sons, New York:349-362. McCall, B., 1954. Are our weeds becoming more resistant to herbicides? Hawaiian Sugar Technology Rep: 146.
- Melander, A.L., 1914. Can insects become resistant to sprays? J. Economic Entomology. 7:167-172.
- Moss, S.R., and Kemp, M.S., 1989. The occurrence of herbicide-resistant weeds in the United Kingdom, with particular reference to Alopecurus myosuroides. CEC. Proc. of Meeting of EC Experts' Group, Tollose, Denmark, 1988. (In press).
- Murphy, K.J., 1983. Herbicide resistance in weeds: a growing problem. Biologist. 34, 4:211-219.
- Pfeiffer, R.K., 1956. Comment in Discussion. Proc. Third British Weed Control Conference 1956, 1:204.
- Putwain, P.D., 1982. Herbicide resistance in weeds - an inevitable consequence of herbicide use? Proc. 1982 British Crop Protection Conference - Weeds:719-728.
- Radosevich, S.R., and Holt, J.S., 1984. In: Weed Ecology - Implications for vegetation management. Wiley and Sons, New York:73-74.
- Robinson, D.W., 1989. Prevention of herbicide-resistant weeds by a policy of zero tolerance. CEC. Proc. of Meeting of EC Experts' Group. Tollose, Denmark, 1988. (In press).
- Rubow, T., 1989. Triazine resistant weeds, Conyza canadensis and Epilobium ciliatum - importance and control in young conifer plantations. CEC. Proc. of Meeting of EC Experts' Group. Tollose, Denmark, 1988. (In press).
- Ryan, G.F., 1970. Resistance of common groundsel to simazine and atrazine. Weed Science, 18:614-616.
- Sovljanski, R., Arsenovic, M and Klokocar Smit, Z., 1989. Herbicide resistant weeds and search for biocontrol agent in Yugoslavia. CEC. Proc. of Meeting of EC Expert's Group. Tollose, Denmark, 1988. (In press).
- Van Himme, M., 1988. Le desherbage chimique des vergers des pommiers et poiriers au printemps et en ete 1988. Le Fruit Belge, 56(421):20-24.
- Van Oorschot, J.L.P., 1989. Chloroplastic resistance of weeds to triazines in the Netherlands until 1988. CEC. Proc. of Meeting of EC Expert's Group, Tollose, Denmark, 1988. (In press).
[* Footnote. Since this article was written, the
herbicide, simazine, has been banned in Europe under Commission Decisions
2004/141/EC(3), 2004/248/EC(4), 2004/140/EC(5) and 2004/247/EC(6), taken within
the framework of Council Directive 91/414/EEC of 15 July 1991. This came into
effect on 26th April 2004.]
[* Footnote. Since this article was written, the herbicide, simazine, has been banned in Europe under Commission Decisions 2004/141/EC(3), 2004/248/EC(4), 2004/140/EC(5) and 2004/247/EC(6), taken within the framework of Council Directive 91/414/EEC of 15 July 1991. This came into effect on 26th April 2004.]
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