Section 8. Pyrethroid resistance: field resistance mechanisms

1993 ◽  
Vol 1 ◽  
pp. 54-61 ◽  
Author(s):  
Neil W. Forrester ◽  
Matthew Cahill ◽  
Lisa J. Bird ◽  
Jacquelyn K. Layland
Keyword(s):  
Selection Pressure ◽  
Pyrethroid Resistance ◽  
Life Stage ◽  
Resistance Mechanism ◽  
Resistance Mechanisms ◽  
Field Resistance ◽  
Monooxygenase System ◽  
Phenotypic Resistance ◽  
Nectar Feeding ◽  
Selection Of

SummaryThe 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.

Section 3. Evaluation of the impact of the strategy on pyrethroid resistance: F1 analyses

1993 ◽  
Vol 1 ◽  
pp. 21-27
Author(s):  
Neil W. Forrester ◽  
Matthew Cahill ◽  
Lisa J. Bird ◽  
Jacquelyn K. Layland
Keyword(s):  
Pyrethroid Resistance ◽  
Resistance Mechanism ◽  
Resistance Management ◽  
Resistance Mechanisms ◽  
Field Resistance ◽  
Relative Importance ◽  
Oxidative Resistance ◽  
Tolerance Curve ◽  
The Impact ◽  
Selection Of

SummaryThe 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.

scholarly journals Evolution of cross-resistance to medical triazoles in Aspergillus fumigatus through selection pressure of environmental fungicides

2017 ◽  
Vol 284 (1863) ◽  
pp. 20170635 ◽  
Author(s):  
Jianhua Zhang ◽  
Joost van den Heuvel ◽  
Alfons J. M. Debets ◽  
Paul E. Verweij ◽  
Willem J. G. Melchers ◽  
...  
Keyword(s):  
Aspergillus Fumigatus ◽  
Selection Pressure ◽  
Target Genes ◽  
Evolutionary Dynamics ◽  
Resistance Mechanism ◽  
Cross Resistance ◽  
Resistance Selection ◽  
Patients At Risk ◽  
Selection Of ◽  
Selection Of Resistance

Resistance to medical triazoles in Aspergillus fumigatus is an emerging problem for patients at risk of aspergillus diseases. There are currently two presumed routes for medical triazole-resistance selection: (i) through selection pressure of medical triazoles when treating patients and (ii) through selection pressure from non-medical sterol-biosynthesis-inhibiting (SI) triazole fungicides which are used in the environment. Previous studies have suggested that SI fungicides can induce cross-resistance to medical triazoles. Therefore, to assess the potential of selection of resistance to medical triazoles in the environment, we assessed cross-resistance to three medical triazoles in lineages of A. fumigatus from previous work where we applied an experimental evolution approach with one of five different SI fungicides to select for resistance. In our evolved lines we found widespread cross-resistance indicating that resistance to medical triazoles rapidly arises through selection pressure of SI fungicides. All evolved lineages showed similar evolutionary dynamics to SI fungicides and medical triazoles, which suggests that the mutations inducing resistance to both SI fungicides and medical triazoles are likely to be the same. Whole-genome sequencing revealed that a variety of mutations were putatively involved in the resistance mechanism, some of which are in known target genes.

scholarly journals Absence of knockdown mutations in pyrethroid and DDT resistant populations of the main malaria vectors in Colombia

2019 ◽  
Vol 18 (1) ◽  
Author(s):  
Lorena I. Orjuela ◽  
Diego A. Álvarez-Diaz ◽  
Juliana A. Morales ◽  
Nelson Grisales ◽  
Martha L. Ahumada ◽  
...  
Keyword(s):  
Insecticide Resistance ◽  
Pyrethroid Resistance ◽  
Resistance Mechanism ◽  
Point Mutations ◽  
Resistance Mechanisms ◽  
Malaria Vectors ◽  
Anopheles Darlingi ◽  
Metabolic Resistance ◽  
Pyrethroid Insecticides ◽  
Voltage Gated Sodium Channels

Abstract Background Knockdown resistance (kdr) is a well-characterized target-site insecticide resistance mechanism that is associated with DDT and pyrethroid resistance. Even though insecticide resistance to pyrethroids and DDT have been reported in Anopheles albimanus, Anopheles benarrochi sensu lato (s.l.), Anopheles darlingi, Anopheles nuneztovari s.l., and Anopheles pseudopunctipennis s.l. malaria vectors in Latin America, there is a knowledge gap on the role that kdr resistance mechanisms play in this resistance. The aim of this study was to establish the role that kdr mechanisms play in pyrethroid and DDT resistance in the main malaria vectors in Colombia, in addition to previously reported metabolic resistance mechanisms, such as mixed function oxidases (MFO) and nonspecific esterases (NSE) enzyme families. Methods Surviving (n = 62) and dead (n = 67) An. nuneztovari s.l., An. darlingi and An. albimanus mosquitoes exposed to diagnostic concentrations of DDT and pyrethroid insecticides were used to amplify and sequence a ~ 225 bp fragment of the voltage-gated sodium channels (VGSC) gene. This fragment spanning codons 1010, 1013 and 1014 at the S6 segment of domain II to identify point mutations, which have been associated with insecticide resistance in different species of Anopheles malaria vectors. Results No kdr mutations were detected in the coding sequence of this fragment in 129 samples, 62 surviving mosquitoes and 67 dead mosquitoes, of An. darlingi, An. nuneztovari s.l. and An. albimanus. Conclusion Mutations in the VGSC gene, most frequently reported in other species of the genus Anopheles resistant to pyrethroid and DDT, are not associated with the low-intensity resistance detected to these insecticides in some populations of the main malaria vectors in Colombia. These results suggest that metabolic resistance mechanisms previously reported in these populations might be responsible for the resistance observed.

scholarly journals Transcriptome analysis of Spodoptera litura reveals the molecular mechanism to pyrethroids resistance

2019 ◽  
Author(s):  
Dongzhi Li ◽  
Yu Mei ◽  
Runqiang Liu ◽  
Xiling Chen ◽  
Li Xu ◽  
...  
Keyword(s):  
Spodoptera Litura ◽  
Pyrethroid Resistance ◽  
Resistance Mechanism ◽  
Resistance Mechanisms ◽  
Agricultural Pest ◽  
Susceptible Population ◽  
Expression Levels ◽  
Kegg Pathways ◽  
Qrt Pcr ◽  
Go Terms

Abstract Background Spodoptera litura is a destructive agricultural pest and has evolved resistance to multiple insecticides, especially pyrethroids. At present, the resistance mechanism to pyrethroids remains unclear.Results Four field-collected populations, namely CZ, LF, NJ and JD, were identified to have high resistance to pyrethroids comparing to pyrethroid-susceptible population (GX), with increased resistant ratio ranging from 40.8 to 1764.0-fold. To characterize pyrethroid resistance mechanism, the transcriptomes between pyrethroid-resistant (LF and NJ) and pyrethroid-susceptible (GX) populations were compared by RNA-sequencing. Results showed that multiple differentially expressed genes were enriched in metabolism-related GO terms and KEGG pathways. 35 up-regulated metabolism-related genes were screened to verify by qRT-PCR. Consistent up-regulation of 13 unigenes, including 3 P450s, 4 GSTs, 1 UGT, 4 COEs and 1ABC, were verified in the additional pyrethroid resistant populations CZ and JD. The expression levels of CYP3 and GST3 , which were homologous to CYP321A8 and GST1 , respectively, showed positive correlation with their pyrethroid resistance levels within CZ, LF, NJ and JD populations. While the expression levels of CYP12 , CYP14 , COE4 and ABC5 showed good correlation with their pyrethroid resistance levels in at least three populations. UGT5 had the highest expression level among the tested UGT genes in the four pyrethroid resistant populations.Conclusion CYP3 , CYP12 , CYP14 , GST3 , COE4 , UGT5 and ABC5 play important roles in pyrethroid resistance among the four field-collected populations. Our work provides a valuable clue for further study of pyrethroid resistance mechanisms in S. litura .

Possible role for wild genotypes of Pisum spp. to enhance ascochyta blight resistance in pea

1998 ◽  
Vol 38 (5) ◽  
pp. 469 ◽  
Author(s):  
J. M. Wroth
Keyword(s):  
Hypersensitive Response ◽  
Ascochyta Blight ◽  
Resistance Mechanism ◽  
Resistance Mechanisms ◽  
Effective Field ◽  
Field Resistance ◽  
Mycosphaerella Pinodes ◽  
Wild Type ◽  
Sources Of Resistance ◽  
The Cross

Summary. There are no cultivars with effective field resistance to ascochyta blight currently available in Australia but a number of wild genotypes of Pisum have been identified as possible sources of resistance and these were evaluated in crosses with a commercial cultivar. Pisum fulvum JI 1006, used as the pollen parent, was crossed with P. sativum cv. Wirrega using wild type P. sativum JI 252 as a bridging cross. JI 1006 and JI 252 both respond to Mycosphaerella pinodes infection by inducing a rapid hypersensitive response. All F2 seedlings (17–20-day-old) from the cross Wirrega × (JI 252 × JI 1006) were screened for their responses to M. pinodes infection in a controlled environment and plants with the highest levels of resistance were then screened as F3 progeny families in the field to determine their responses to natural M. pinodes infection. Nine percent of these families were significantly more resistant for both leaf and stem disease compared with Wirrega and among them were 9 lines which flowered at the same time or earlier than Wirrega. However, even the most resistant line had 30% of the foliage destroyed by disease, indicating disease control was insufficient. A second resistance mechanism which impeded M. pinodes hyphal penetration in leaves (P. sativum SA 1160) was combined with the hypersensitive response in the cross SA 1160 × (JI 252 × JI 1006). The level of resistance to disease was now significantly higher than any plant in the original F3 population, despite the wild-type growth habit of these plants. It is suggested that breeding programs should focus first on maximising field resistance through isolation of some optimal combinations of resistance mechanisms in wild genotypes before turning to improving the agronomic performance through backcrossing to advanced breeding lines.

scholarly journals Transcriptome analysis of molecular mechanism to pyrethroids resistance in Spodoptera litura

2019 ◽  
Author(s):  
Dongzhi Li ◽  
Yu Mei ◽  
Jianhua Wang ◽  
Xiling Chen ◽  
Chengju Wang ◽  
...  
Keyword(s):  
Spodoptera Litura ◽  
Pyrethroid Resistance ◽  
Resistance Mechanism ◽  
Resistance Mechanisms ◽  
Expression Level ◽  
Resistance Level ◽  
Kegg Pathways ◽  
Qrt Pcr ◽  
Differential Expressed Genes ◽  
Go Terms

Abstract Background Spodoptera litura is a destructive agricultural pest and had evolved resistance to multiple insecticides, especially pyrethroids. At present, the resistance mechanism to pyrethroids remains unclear. Results Four field-collected populations, namely CZ, LF, NJ and JD, were identified to have high resistance to pyrethroids, and the resistant ratio ranged from 40.8 to 1764.0-fold. To explore pyrethroids resistance mechanism, the transcriptome between pyrethroid-resistant (LF and NJ) and pyrethroid-susceptible (GX) populations were compared by RNA-sequence. Results showed that multiple differential expressed genes were enriched in metabolism-related GO terms and KEGG pathways. 35 up-regulated metabolism-related genes were screened to verify by qRT-PCR. Consistent up-regulation of 13 unigenes, including 3 P450s, 4 GSTs, 1 UGTs, 4 COEs and 1ABC, were verified in the additional pyrethroids resistant populations CZ and JD. The expression level of CYP3 and GST3, which were homologous to CYP321A8 and GST1, respectively, showed good correlation with their pyrethroids resistance level among CZ, LF, NJ and JD populations. While the expression level of CYP12, CYP14, COE4 and ABC5 showed good correlation with their pyrethroids resistance level in at least three populations. UGT5 had the highest expression level among the tested UGT genes in the four pyrethroids resistant populations. Conclusion CYP3, CYP12, CYP14, GST3, COE4, UGT5 and ABC5 play important roles in pyrethroids resistance among the four field-collected populations. Our study provided a valuable resource for further study of pyrethroid resistance mechanisms in S. litura.

scholarly journals Escalation of Pyrethroid Resistance in the Malaria Vector Anopheles funestus Induces a Loss of Efficacy of Piperonyl Butoxide–Based Insecticide-Treated Nets in Mozambique

2019 ◽  
Vol 220 (3) ◽  
pp. 467-475 ◽  
Author(s):  
Jacob M Riveron ◽  
Silvie Huijben ◽  
Williams Tchapga ◽  
Magellan Tchouakui ◽  
Murielle J Wondji ◽  
...  
Keyword(s):  
Cytochrome P450 ◽  
Pyrethroid Resistance ◽  
Anopheles Funestus ◽  
Resistance Mechanisms ◽  
Piperonyl Butoxide ◽  
Insecticide Treated Nets ◽  
Molecular Analyses ◽  
Cytochrome P450 Genes ◽  
High Degree ◽  
Long Lasting Insecticidal Nets

Abstract Background Insecticide resistance poses a serious threat to insecticide-based interventions in Africa. There is a fear that resistance escalation could jeopardize malaria control efforts. Monitoring of cases of aggravation of resistance intensity and its impact on the efficacy of control tools is crucial to predict consequences of resistance. Methods The resistance levels of an Anopheles funestus population from Palmeira, southern Mozambique, were characterized and their impact on the efficacy of various insecticide-treated nets established. Results A dramatic loss of efficacy of all long-lasting insecticidal nets (LLINs), including piperonyl butoxide (PBO)–based nets (Olyset Plus), was observed. This An. funestus population consistently (2016, 2017, and 2018) exhibited a high degree of pyrethroid resistance. Molecular analyses revealed that this resistance escalation was associated with a massive overexpression of the duplicated cytochrome P450 genes CYP6P9a and CYP6P9b, and also the fixation of the resistance CYP6P9a_R allele in this population in 2016 (100%) in contrast to 2002 (5%). However, the low recovery of susceptibility after PBO synergist assay suggests that other resistance mechanisms could be involved. Conclusions The loss of efficacy of pyrethroid-based LLINs with and without PBO is a concern for the effectiveness of insecticide-based interventions, and action should be taken to prevent the spread of such super-resistance.

scholarly journals Characterization of resistance mechanisms of Enterobacter cloacae Complex co-resistant to carbapenem and colistin

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Shixing Liu ◽  
Renchi Fang ◽  
Ying Zhang ◽  
Lijiang Chen ◽  
Na Huang ◽  
...  
Keyword(s):  
Lipid A ◽  
Efflux Pump ◽  
Resistance Mechanism ◽  
Carbapenem Resistance ◽  
Enterobacter Cloacae ◽  
Resistance Mechanisms ◽  
Colistin Resistance ◽  
Carbapenem Resistant ◽  
Horizontal Spread

Abstract Background The emergence of carbapenem-resistant and colistin-resistant ECC pose a huge challenge to infection control. The purpose of this study was to clarify the mechanism of the carbapenems and colistin co-resistance in Enterobacter cloacae Complex (ECC) strains. Results This study showed that the mechanisms of carbapenem resistance in this study are: 1. Generating carbapenemase (7 of 19); 2. The production of AmpC or ESBLs combined with decreased expression of out membrane protein (12 of 19). hsp60 sequence analysis suggested 10 of 19 the strains belong to colistin hetero-resistant clusters and the mechanism of colistin resistance is increasing expression of acrA in the efflux pump AcrAB-TolC alone (18 of 19) or accompanied by a decrease of affinity between colistin and outer membrane caused by the modification of lipid A (14 of 19). Moreover, an ECC strain co-harboring plasmid-mediated mcr-4.3 and blaNDM-1 has been found. Conclusions This study suggested that there is no overlap between the resistance mechanism of co-resistant ECC strains to carbapenem and colistin. However, the emergence of strain co-harboring plasmid-mediated resistance genes indicated that ECC is a potential carrier for the horizontal spread of carbapenems and colistin resistance.

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