In response to field pyrethroid failures against Helicoverpa armigera (Hübner) in early 1983, an insecticide resistance management (IRM) strategy was introduced for insect control in summer crops in eastern Australia. The aims of this strategy were to contain the pyrethroid resistance problem, to prevent re-selection of historical endosulfan resistance (both curative IRM) and to avoid any future problems with organophosphate/carbamate resistance (preventative IRM). An alternation strategy was adopted which was based on the rotation of unrelated chemical groups on a per generation basis, along with a strong recommendation for the use of ovicidal mixtures. These chemical countermeasures were then integrated with other non-chemical control methods (biological and cultural) into a workable integrated pest management programme. The restrictions were applied to all Helicoverpa armigera susceptible crops (including cereals, oilseeds, grain legumes, tomatoes, tobacco and cotton) and even to other co-incident pest species. From its inception, compliance with the voluntary strategy has been exceptional.

The monitoring technique employed in this study (discriminating dose screening of larvae reared from field collected eggs) proved extremely successful in documenting the impact of the strategy on both pyrethroid and endosulfan resistance, without the problems of alternative techniques. Because of the sensitivity of this technique, strategy users have been able to verify the anticipated impact of the strategy, identify problems, adjust their management practices accordingly and assess the effectiveness of these procedures. This has resulted in the maintenance of the strategy's excellent compliance rate.

Pyrethroids imposed selection for resistance in both moths and larvae, resulting in increases in resistance within the Stage II window and the early Stage III period, respectively. These two peaks effectively merged into one large peak while the period of pyrethroid use remained at 42 days. However, the initiative to reduce the pyrethroid window to 35 days separated the two peaks and proved to be a successful delaying tactic. The two main factors influencing pyrethroid resistance appear to be dilution by susceptibles immigrating from the refugia, followed by pyrethroid selection pressure. However, as the refugia became increasingly contaminated, their effectiveness as a source of susceptibles for dilution declined, resulting in gradually increasing pyrethroid resistance levels in all areas over time. Adult selection was more important in the mixed crop Emerald study area because of premating selection. This, along with the higher Helicoverpa armigera pressure at Emerald, probably offset any potential benefit of the longer crop season at this site. Inadequate cultivation of post-harvest fields harbouring overwintering pupae, presumably due to low price forecasts in the economically sensitive cotton industry, resulted in the survival of large numbers of resistant pupae. As a result, cultural control of overwintering pupae has become a major component of the integrated Australian resistance management strategy. The strategy has not overcome the pyrethroid resistance problem but has proved to be a successful delaying tactic in ‘buying time’ and extending the useful life of the pyrethroids.

However, the strategy has been much more successful in managing endosulfan resistance and some possible reasons for this are discussed: effectively lower selection pressure, fitness deficit, fewer life stages selected, or lower genetic dominance. However, it was not possible from this study to determine the relative importance of these factors or their interactions.

The classical resistance monitoring technique using full bioassay lines on laboratory reared F1 progeny of field material was compared to the previously described discriminating dose technique on field collected individuals. The Via tolerance curve analysis of the F1 data clearly indicated the predominance of the oxidative metabolic pyrethroid resistance mechanism from the 1984/85 season onwards. There appears to have been an abrupt change in the relative importance of field resistance mechanisms following the introduction of the insecticide resistance management (IRM) strategy in 1983/84. The strategy seems to have favoured the selection of the more amenable oxidative resistance mechanism over the intractable nerve insensitivity mechanism. The Beeman-Nanis analysis was applied to attempt to identify the relative importance of the various field resistance genes. However, it proved of little value in this study as one of the key assumptions underlying the analysis (full genetic dominance) was not satisfied.

Resistance to endosulfan and pyrethroids in Helicoverpa armigera in Australia was shown to be due to multiple rather than cross resistance. The independence of the endosulfan and pyrethroid resistance mechanisms vindicates the sequential use of these two groups in Stages I and II of the insecticide resistance management strategy, respectively. Within the cyclodienes, greatest resistance occurred to dieldrin with lower order cross resistance to endosulfan and endrin. Male and female moths expressed cyclodiene resistance equally.

Both pyrethroid and endosulfan resistant Helicoverpa armigera larvae were shown to have marginally longer development times. Pyrethroid resistant larvae were slower developers often requiring an extra moult before ultimately pupating to the same size pupa as susceptibles. There were no differences between pyrethroid resistant and susceptible pupal development times (male or female). Laboratory and field competition studies could demonstrate no selective advantage for either pyrethroid resistant or susceptible larvae or prepupae. Thus it would seem that the slightly longer larval development times do not manifest as significant biological deficits. This helps explain the gradually deteriorating pyrethroid resistance situation documented during evaluation of the Australian insecticide resistance management (IRM) strategy. There was no evidence of the selection of fitness modifiers (co-adaptation) to overcome the slower development of either pyrethroid or endosulfan resistant larvae. Endosulfan fitness disadvantages were not sufficiently researched in this study to discount the possibility of a fitness deficit contributing to the much more successful management of endosulfan resistance.

Pyrethroids applied to flowering sorghum, at either the low midge rate or the higher Helicoverpa rate (20 g and 100 g fenvalerate a.i./ha, respectively), caused selective mortality of Helicoverpa armigera larvae and resulted in differential selection for resistance. This finding vindicated the original strategy decision to apply the same temporal restrictions on pyrethroid use for sorghum midge, Contarinia sorghicola, as those for H. armigera.

Adult Helicoverpa armigera were shown to be capable of expressing pyrethroid resistance to both direct and indirect exposure. Male and female moths were equally resistant. Pyrethroid field sprays selected for resistance in moths which were repelled onto neighbouring unsprayed cotton and possibly also, lower into the unsprayed portion of the canopy. Selection of moths prior to egg laying is suggested as the explanation for the immediate increase in pyrethroid resistance which occurs within the Stage II window.

The phenotypic expression of pyrethroid resistance in adult H. armigera declined significantly with age, beginning sometime between four and six days and continuing for the effective life span of the moth. This was the main reason for the poor correlation of adult resistance (determined from pheromone trapped males) and resistance in field collected eggs found in a detailed study comparing both techniques on two properties. On a young emerging moth population, pyrethroids remained selective for four to five days. On an ageing population, pheromone trapped males significantly underestimated resistance. Endosulfan and profenofos sprays were neutral in their impact on pyrethroid resistance in both eggs and adults. The resistance peaks in eggs lagged four to seven days behind the pyrethroid applications. The advantages and disadvantages of monitoring resistance using pheromone trapped males are discussed.

The dual insecticide ± synergist discriminating dose technique proved highly successful in determining the relative importance of pyrethroid resistance mechanisms present in field populations of Helicoverpa armigera, without the problems of alternative techniques. Synergist pre-treatment proved unnecessary therefore allowing use of the more convenient and labour efficient discriminating dose pre-mix.

Oxidative metabolic detoxification, probably via a polysubstrate monooxygenase system, was the major pyrethroid resistance mechanism in both larval and adult H. armigera. Residual piperonyl butoxide insensitive resistance (presumably nerve insensitivity, possibly acting in combination with the penetration resistance factor) was also present but at a low level. This latter resistance mechanism was expressed in larvae but moths appeared to express only weak phenotypic resistance. The predominant pyrethroid resistance mechanism employed by insects is discussed in relation to their feeding habit. The tenet that nectar feeding adult Lepidoptera are unable to express metabolic pyrethroid resistance is challenged.

Unrestrained pre-strategy pyrethroid selection pressure on sequential generations resulted in selection for elevated levels of kdr type nerve insensitivity and possibly even super kdr. Restriction of pyrethroid selection pressure to one generation per season favoured selection of the oxidative over the nerve insensitivity resistance mechanism. Two possibly complementary explanations are put forward for this; differential genetic dominance (semidominant oxidative mechanism versus recessive nerve insensitivity) and/or selection in more than one life stage (moths and larvae for the oxidative mechanism versus predominantly larvae only for the nerve insensitivity mechanism). It is suggested that insecticide resistance management strategies should be designed to avoid selection of elevated levels of the intractable nerve insensitivity resistance mechanism whereas low levels of this mechanism (normal kdr) are not considered difficult to manage. The demonstration that the strategy has favoured selection of the more amenable oxidative resistance mechanism invites the opportunity to develop possible chemical countermeasures.

Sixty-five synergists and seven solvents were tested on larvae of a pure breeding pyrethroid resistant strain of Helicoverpa armigera (homozygous for a metabolic detoxification mechanism fully suppressible by piperonyl butoxide (Pbo), presumably via a microsomal monooxygenase system). The methylenedioxyphenyl and acetylenic compounds were the most effective synergists with moderate activity from some organophosphate compounds, particularly the N-alkyl phthalimidomethyl phosphorodithioate, phosmet. All the other compounds tested were either ineffective or only marginally effective including the majority of organophosphates (12 out of 18 tested), pyrethroid analogues, N-alkyls, esterase and glutathione transferase inhibitors, various nitrogen heterocycles, juvenile hormone and analogues, formamidines, organochlorines, anti-oxidants and kojic acid. The most promising synergists indicated for further evaluation were synthetic analogues of Pbo, phosmet, propargite and possibly also fenthion, phosalone, azinphos-ethyl, pyrazophos and kinoprene. All solvents (except dodecane) had no impact on improving kill, indicating that the mode of action of Pbo and the other synergists in this study is principally true biochemical inhibition and not quasi-synergism (improved penetration). Dodecane marginally improved kill in the resistant but not the susceptible strain, indicating some preferential penetration synergism in the resistant strain.

A number of trials with Pbo were designed to facilitate the development of this synergist for commercial field use within the Australian IRM strategy. From these, it was found that: 1. A set rate of Pbo should be used, irrespective of the activity of the accompanying pyrethroid. 2. Residual activity of Pbo is poor (less than 50% of initial activity by two days post spray) but that this could be partially overcome by increasing the rate. 3. Straight Pbo applied onto a weathered pyrethroid deposit could restore control but only temporarily and would probably be of little practical field use. 4. No difference in residual activity could be found between the four formulations of Pbo tested. The synthetic analogue PBX was slightly less intrinsically active than the natural product (Pbo) but when tested in the field against Pbo at the same rate, was equivalent in efficacy to both the standard commercial and research Pbo formulations.

In order to preserve the long-term effectiveness of Pbo as a pyrethroid synergist within the Australian IRM strategy, an optimal use strategy (based on synergist rotation within the present insecticide rotation scheme) is proposed.

The structural requirements for designing a resistance breaking pyrethroid to overcome oxidative metabolic pyrethroid resistance in Helicoverpa armigera were studied. A range of pyrethroid structures were tested on a well defined pure breeding pyrethroid resistant strain of H. armigera (homozygous for a metabolic detoxification mechanism fully suppressible by piperonyl butoxide, presumably via a microsomal monooxygenase system). Highest resistance factors were to the ester bonded phenoxybenzyl alcohol pyrethroids, particularly to those with an aromatic acid moiety. Changes to the alcohol moiety alone could overcome most, if not all, resistance. Simple benzyl alcohols were the most effective followed by cyclopentenolones and a methylated biphenyl alcohol. However, the benzylfurylmethyl alcohol (bioresmethrin) was not effective. The incorporation of a synergophore grouping into the alcohol moiety was fully effective for Scott's Py III (methylenedioxyphenyl) and prallethrin (propynyl) but only partially effective for tetramethrin (N-alkyl). Changes to the acid moiety had little effect except for the incorporation of a synergophore methylenedioxyphenyl grouping (Cheminova I) which was just as effective as for the same insertion in the alcohol moiety. The change to a central ether bond from the conventional ester bond lowered resistance. Reversion to an unsubstituted alpha carbon analogue from the conventional alpha cyano group also lowered resistance.

Piperonyl butoxide (Pbo) had little effect on pyrethroid toxicity in the susceptible strain except for the single isomers deltamethrin and esfenvalerate. However, it was more than fully effective in overcoming resistance and actually reduced resistance factors to significantly below one in the resistant strain. This indicated the possibility that Pbo could be acting both as a classical monooxygenase inhibitor and a preferential penetration synergist in resistant larvae.

Partial or full resolution of racemic mixtures had minimal impact on increasing toxicity in the susceptible strain. However, partially or fully resolved isomers were clearly much more toxic on resistant strains, indicating a possible blocking effect of the inactive isomers during the toxication process with the higher pyrethroid doses applied to resistant larvae. Cis isomers had only slightly higher resistance factors than trans isomers.

Seven fully effective resistance breaking pyrethroids were identified in this study and one of these (the simple benzyl alcohol, Series Two) was shown to be equally effective on both adults and larvae of H. armigera. It was also shown to work equally well on laboratory or field material and gave results similar to a pyrethroid/Pbo combination. However, none of the resistance breakers identified so far are able to satisfy all of the requirements necessary for an ideal resistance breaking pyrethroid (i.e. good resistance breaking activity at low rates, photostability, residual activity similar to current pyrethroids and safety to mammals). Factors acting against the possible commercialization of successful resistance breaking compounds are discussed.