This document discusses insecticide resistance in insects. It begins by defining insecticide resistance as the ability of some insects to survive exposure to an insecticide that would normally kill them. The document then discusses the history of reported insecticide resistance dating back to 1914. It notes that over 500 insect species have now developed resistance. The mechanisms of resistance include metabolic resistance, target site resistance, behavioral resistance, and penetration resistance. Factors that influence the development of resistance include the frequency of insecticide application and the intensity of selection pressure from the insecticide.

1. WELCOME
1

2. INSECTICIDE RESISTANCE
TYPES & MECHANISMS
RESURGENCE
Presented by:
Ch. Naga Satyasri
BAM-14-28 2

3. • The added ability to withstand an insecticide,
acquired by breeding of those individuals, which
survive exposure to that particular insecticide
insufficient to wipe out the whole colony.
HOSKINS & GORDON (1956)
• Resistance to insecticide is the development of an
ability in a strain of insects to tolerate doses of
toxicant which would prove lethal to majority of
individuals in a normal population of the same
species.
WORLD HEALTH ORGANISATION (W.H.O.)
Definition
3

4. • The first report of resistance came from Melander in
1914 who found sanjose scale, Quadrispidiotus sp. a
pest of apples resistant to lime sulphur.
• Between 1916 and 1946, ten more cases of resistance
to inorganic pesticides like arsenicals, selenium,
cyanide and other compounds were reported.
• DDT which is patented in 1942, and by 1947,
housefly resistance to DDT was documented.
4

5. • After 1946, successive reports of insecticides
resistance poured in the mosquito become resistant to
DDT (1947) and housefly to pyrethrum (1952) and
parathion (1952).
• By 1962, a list of 150 resistant insects becomes
available and by 1976 the number went up to 300
insects. At present there are over 500 species of
insects were found resistant to one or more
insecticides.
5

6. Year
NumberofResistantspecies
6

7. • The occurrence of resistance to insecticide was first
noticed in India in insects of public health
importance.
• The first report of DDT resistance in mosquitoes came
in 1952, in Culex fatigans a transmitter of filaria
from U.P. and Mumbai.
• Since then this mosquito was resistant to both DDT
and BHC in various parts of the country.
7

8. • Resistance to agricultural pests was first reported by
Pradhan et al., (1963) on singhara beetle, Gelerucella
birmanica in 1963 from Delhi against DDT and BHC.
• Srivastava and Joshi (1965) reported the BHC
resistance in Spodoptera litura from Rajasthan.
• Beside BHC this pest was also developed resistance to
Malathion, Endosulfan
8

9. • The development of resistance in Tribolium
castaneum to lindane and phospene (Kalra et al.1975;
Champ and Dyte, 1976).
• Orzaephilus surinamensis resistant to malathion and
lindane (Champ and Dyte, 1976).
• In Khapra beetle, Dermestis granarium to phosphine
(Borah and Chahal, 1979) has been reported in
different parts of country.
9

10. • Tribolium castaneum ,Ephestia kuehniella and Plodia
interpunctella shows resistance against spinosad
(Maedeh Mollaie, 2011).
• Tribolium castaneum shows resistance against the
lufenuron (Arora M.S., 2012).
10

11. Planting of Bt crops globally and field-evolved
resistance.
11

12. 12

13. 13

14. Resistance is best understood as a process
Initially, a small proportion of population has a resistant
mechanism by chance.
14

15. The Resistance Process
These individuals survive at a higher
rate than others
15

16. Resistance as a process
Resistant individuals increase in
frequency
16

17. Resistance as a process
Eventually, the pesticide or other
management tactic causes too little control to
be effective.
17

18. The process has three general stages, each
with its own Management Strategy
Prevention
Abandon Pesticide/Management Tactic
Need to
monitor
resistance
18

19. 19

20. Number of species of insects and mites
reported resistant to insecticides
Order Chemical group
Cyclodien
es
DDT OP Carbmat
es
Pyrethroids Fumigant
s
Other
Diptera 108 107 62 11 10 - 1
Lepidoptera 41 41 34 14 10 - 2
Coleoptera 57 24 26 9 4 8 5
Homoptera 15 14 30 13 5 3 1
Heteroptera 16 8 6 1 - - -
Others 23 21 9 3 1 - 2
Acarina 16 18 45 13 2 - 27
Total 276 233 212 64 32 11 38
% 66 52 47 14 7 2 9
20

21. Examples of insects that tend to readily develop
resistance to insecticides
Insect Insecticides Resisted
Green peach aphid Neonicotinoids, carbamates, organophosphates,
pyrethroids, cyclodienes
Diamondback moth Many insecticides
Colorado potato beetle Many insecticides
Maize earworm Pyrethroids, cyclodienes, carbamates,
organophosphates
Bed bugs Pyrethroids, cyclodienes, organophosphates
Western root worm Cyclodienes, carbamates, organophosphates, Bt
toxins
Indian meal moth Organophosphates, cyclodienes, Bt toxins,
pyrethrins
Anopheles mosquitoes Many insecticides
Tobacco budworm Many insecticides 21

22. How Resistance Develops…….
• Resistance usually develops by genetic mutations
• Types of mutations can include :
 A change in processes in the pest that make the
pesticide harmless;
 A change in the place where the pesticide enters
the pest so it cannot enter;
 A change in the behaviour of the pest so that it
avoids the pesticide.
22

23.  Insecticide resistance develops in target insects
when a larva carrying a resistance mutation
survives the application of a particular
insecticide - breeds as a resistant insect.
 If a large proportion of the breeding population
is then exposed to an insecticide of the same
group selection for the resistance mutation will
increase population of resistant insects will
increase with time.
•
23

24. Source: McDougall, Sandra (2002) Integrated Pest Management in
Lettuce: Information Guide.
24

25. Types of resistance
– Cross resistance
– Multiple resistance
– Negatively correlated resistance.
25

26. The rate of development of resistance
in a population depends on…..
 The frequency of resistant genes present in a population
 The nature of genes (single or multiple; dominant or
recessive)
 The intensity of the selection pressure of the toxicant
 The rate of breeding of the species
26

27. 27

28. Cross resistance
• It is operated when the same defence mechanism
(usually governed by a single gene pair), such as
increased oxidative detoxification, protects against
several other insecticides.
• The phenomenon of cross resistance is a relatively
frequent one in vector populations. For example, DDT
and pyrethroid insecticides are chemically unrelated
but both act on the same target site, the voltage gated
sodium channel
28

29. • Past use of DDT has resulted in several insect
species developing resistance to DDT due to
the kdr (Knock down resistant) mutation at
the target site.
• Where these mutations have been retained in
the population, the insects have some
resistance to all pyrethroids in addition to
DDT. Cross resistance can also occur between
OP and carbamate insecticides when resistance
results from altered AChE
29

30. Multiple resistance
• It occurs when resistance to various chemicals
conferred by different coexisting defence
mechanisms in the same insect strain, with
each mechanism apparently coded by a
different gene rather than all mechanisms
controlled by a pleotropic expression of the
same gene.
30

31. • Localized populations of Colorado potato
beetle are notorious for multiple resistance to
more than 50 insecticides with various modes
of action.
31

32. Negatively correlated resistance
• Selection of resistance by pressure from
insecticide ‘A’ leads to a corresponding
selection of susceptibility to insecticide ‘B’ vice
versa.
• Thus, insect species which do not kill by ‘A’
can be controlled by ‘B’ for a few years,
therefore alternate use of insecticide ‘A’ and ‘B’
can be utilized for pest suppression for a
longer period. 32

33. Mechanisms of resistance
• There are several ways that insect populations
can become resistant to insecticides, and pests
may exhibit more than one of these
mechanisms at the same time.
• Metabolic resistance is the most common type
of resistance. Insects possess a variety of
enzymes, including oxidases, glutathione S-
transferases, esterases and amidases, whose
function is to degrade foreign compounds.
33

34. • Resistance to a toxicant can occur when the insects
evolve an enhanced ability to detoxify or destroy the
toxin, by alterations of these enzymes or of the
amounts of enzymes produced in the body.
• As metabolic enzymes are directed at certain
structural features of the toxicants, vulnerable sites in
the molecule are affected.
• This type of resistance may not affect all members of
a chemical class, and cross-resistance between
compounds from different chemical classes can occur
if they contain common chemical groups that are
targeted by the same enzyme.
34

35. Metabolic resistance
• Resistant insects may detoxify or destroy the
toxin faster than susceptible insects, or prevent
the toxin from reaching target sites by binding
it to proteins in their bodies.
• Metabolic resistance is the most common
mechanism.
• Resistant insects may possess higher levels or
more efficient forms of the enzyme(s) that
break down insecticides to nontoxic
compounds. 35

36. 36

37. Altered target-site resistance
• The site where the toxin usually binds in
the insect becomes modified to reduce the
insecticide's effects.
• Chitin is a major component of an insect's
exoskeleton.
37

38. In the following example, enzyme H is necessary for
chitin production.
(i) To prevent moulting, the insecticide
binds with the target site
(ii) In a resistant insect,
the target site is altered
(iii) and prevents the insecticide from
binding with the enzyme
38

39. Behavioral resistance
• Resistant insects may avoid the toxin by a
change from their normal activity.
• Insects may simply stop feeding or move to the
underside of a sprayed leaf.
• Some malaria-transmitting mosquitoes in
Africa developed a preference for resting
outside that prevented them from coming in
contact with pesticide sprayed on interior
walls. 39

40. Penetration resistance
• Resistant insects may absorb the toxin more slowly
than susceptible insects.
• Penetration resistance occurs when the insect’s outer
cuticle develops barriers which can slow absorption
of the chemicals into their bodies.
• This mechanism is frequently present along with
other types.
40

41. Resistant insect
Susceptible insect
41

42. Major biochemical mechanisms conferring resistance to important
classes of insecticides in adult mosquitoes.
Circle size reflects the relative impact of the mechanism on resistance
42

43. Major factors that influence resistance
development
• Frequency of application :
• How often an insecticide or control tactic is
used is one of the most important factors that
influence resistance development.
• With each use, an advantage is given to the
resistant insects within a population.
43

44. • Dosage and persistence of effect :
• The length of time that an insecticide remains
effective, also called its persistence, is
dependent upon the physical chemistry of the
insecticide, the type of formulation, and the
application rate.
• Products which provide a persistent effect
provide continual selection pressure in a
similar manner to multiple treatments.
• It is important to always follow manufacturer
and WHO recommendations when using
insecticides.
44

45. • Rate of reproduction :
• Insects that have a short life cycle and high rates of
reproduction are likely to develop resistance more rapidly
than species which have a lower rate of reproduction, as
any resistance genes can rapidly spread throughout the
population.
• Mosquitoes have a history of insecticide resistance and
are characterised by a relatively short life cycle and high
fecundity, with females laying several hundred eggs
during their reproductive life.
• In contrast, the tsetse fly is less likely to develop resistance
to insecticides due to a longer life cycle and relatively low
rate of reproduction, females producing in total fewer
than 10 offspring.
45

46. Insecticide resistance detection
methods
1) Conventional Detection Methods
2)Biochemical detection of insecticide resistance
3) Immunological Detection Methods
4)Detection of monooxygenase (cytocrome
P450) based insecticide resistance.
46

47. Conventional Detection Methods
• Larvae or adults are tested for resistance by
assessing their mortality after exposure to a
range of doses of an insecticide.
• For susceptible and field populations, LD50 or
LC50 values were calculated by using probit
analysis.
47

48. Biochemical detection of insecticide
resistance
• Biochemical assays/techniques may be used to
establish the mechanism involved in resistance.
• When a population is well characterised some
of the biochemical assays can be used to
measure changes in resistance gene
frequencies in field populations under
different selection pressure.
48

49. Immunological Detection Methods:
• This method is available only for specific elevated
esterases in collaboration with laboratories that have
access to the antiserum.
• There are no monoclonal antibodies, as yet, available
for this purpose.
• An antiserum has been prepared against E4
carboxylesterase in the aphid Myzus persicae .
• An affinity purified 1gG fraction from this antiserum
has been used in a simple immunoassay to
discriminate between the three common resistant
variants of M. persicae found in the UK field
populations (Devonshire et al, 1996).
49

50. Detection of monooxygenase (cytocrome P450)
based insecticide resistance.
• The levels of oxidase activity in individual
pests are relatively low and no reliable assay
has been developed to measure p450 activity
in single insects.
• The p450s are also a complex family of
enzymes, and it appears that different
cytocromes p450s produce resistance to
different insecticides.
50

51. Impact of Resistance
• Overall agricultural productivity (during build
phase)
– Increased pesticide usage
– Increased damage
• Environmental impact
– Increased pesticide usage
– Increased use of non-renewable resources
– Increased acreage
• Pest management flexibility
– Loss of pesticide tactic
– Constraint on new pesticides
51

52. Solution to the problem of resistance
1. Occasional change of insecticide
2. Use of undetoxifiable analogues
3. Mixtures and alternations
4. Negatively correlated insecticides
5. Development of newer insecticides
6. Use of insect pheromones
7. Use of insect hormones
8. Use of integrated approach
9. Use of synergists
52

53. Judicious use of insecticide
 Indiscriminate use of insecticides lead to the
development of resistance.
 Need based insecticidal spray should be taken up
when pest population reaches the economic thresh-
hold level.
 Selective insecticides should be sprayed using proper
dose and right equipment.
53

54. Mixtures and Alteration of insecticide:
One of the counter measure for resistance for one
insecticide is to switch to another insecticide preferably
belonging to different group.
Examples
 There are reports stating DDT resistance in the housefly
countered by substituting lindane or dieldrin
 In India Heliothis armigera infesting cotton developed
resistance against synthetic pyrethroids which could be
countered by substituting acephate.
54

55. Use of undetoxifiable analouges:
 Use of two insecticides of independent action in a
mixture against the resistant strain gives a good control
and delays the development of resistance.
Examples:
 In cotton white flies developed against synthetic
pyrethroids the mixture of cypermethrin and
profenophos is used for overcoming the problem .
 DDT analogues such as prolan and Butalan
(commercial mixture- Dilan) lacking terminal
chlorination on the central aliphatic chain are not
easily detoxified by resistant strains. 55

56. Use of synergist
 Synergist enhances the toxicity of a given insecticide
by inhibiting the detoxification mechanism.
 The first synergist was introduced in 1940 to increase
the effectiveness of pyrethrum. The mode of action of
synergist is the inhibition of mixed function oxidase
enzymes that metabolize insecticides.
 Resistance to OP compounds, carbamates and
pyrethrum are overcome by use of synergists such as
piperonyl butoxide
56

57.  Malathion resistance overcome by use of synergists
such as triphenyl phosphate and tributyl
phosphorotrithioate.
 Piperonyl butoxide and other methylene dioxyphenyl
compounds serve to synergize many insecticides like
DDT, carbamates etc., against houseflies and other
insect pests.
 Propyl-paraoxon synergizes malathion and parathion
through inhibition of phosphatase.
57

58. Negatively correlation insecticides
 Specific resistance to one insecticide leads to
enhanced susceptibility to another insecticide.
 Cyclodiene resistant boll weevil have been found
more susceptible to malathion
58

59. Development of newer insecticides:
 Switching over to newly evolved insecticide or to
microbial insecticide is an important counter measure
for delaying resistance.
Use of insect pheromones
 Pheromone regulate insect behaviour and hormones
regulate growth and reproduction. These can used
successfully against resistance strains; use of sex
pheromones
59

60. Use of integrated approaches
 An integrated approach to control of insect pests will
reduce the application of insecticides, which in turn,
will lower insecticide pressure on insects.
 Under such condition genes governing resistance may
not get activated or may take longer time to do so and
keep resistance postponed for some time
60

61. • RESISTANCE MANAGEMENT STRATEGY DESIGN
• Crop/Pest or Regional Strategies
The strategies are provided on a CROP by PEST basis
In many cases, a specific MoA insecticide can be used
across this range of crops to control multiple pests that
have the ability to move from crop to crop.
The overall Resistance Management Strategy of
avoiding overuse of individual Modes of Action
insecticides should be followed, not just on a specific
crop and pest but on a broad perspective of crops and
pest complex. 61

62. Crop(s) : Sorghum, Maize, Summer Grain Legumes
Insect(s) : Cotton bollworm/Native budworm (Helicoverpa)
spp.)
 Monitor pest levels and do not spray unless pest thresholds are
reached.
 Do not use consecutive applications of products from the same
chemical group in Stages II and III.
62

63.  In maize the critical stage of infestation- silking.
Infestation could extend through to when the grain in
cobs begins to harden although spraying for Heliothis is
generally not required after silking is complete.
 In sorghum the critical stage of infestation-flowering and
milky dough stage. Infestation could extend through to
when the grain begins to harden.
 Post-harvest cultivation to destroy pupae, as practised in
cotton crops, should also be practised in sorghum, maize
and grain legume crops.
63

64. Conclusions:
• Resistance is caused by evolution — a fundamental
biological process.
• The biochemical and physiological mechanisms may
be many, but resistance is often due to an insensitive
target for the pesticide or to increased detoxication.
• It is possible to curb or delay resistance development
by making reproduction better for populations or
subpopulations of pests that are not under selection
pressure.
64

65. • Cross-resistance may occur for pesticides with
related modes of action, but sometimes also
between nonrelated pesticides if they can be
detoxified by the same enzyme.
65

66. Insecticide-resurgence
66

67. Definition
Population after having been suppressed rebounds to
numbers greater than before suppression occurred
(Pedigo, 1989)
Increase in target arthropod ‘pest’ species abundance to a
level which exceeds that of a control or untreated
population following the application of an insecticide
( Hardin et al., 1995)
67

68. • It is defined as an abnormal increase of pest population often
exceeding the economic injury threshold, following insecticide
treatment (Chelliah, 1979).
• Heinrich et al 1982 defined resurgence as a statistically
significant increase in the insect population or damage in
insecticide treated plots over that of untreated plots.
68

69. Historical perspective:
• The first instance of resurgence in rice was noticed in
Brown plant hopper in the experimental fields of the
IRRI.
• where the plots treated with gamma HCH @ 2 kg ai
/ha recorded approximately three times higher
population of BPH than the untreated control (IRRI,
1969).
• Resurgence has become a wide spread phenomenon
in the past 2 decades (Bhathal et al., 1991).
69

70. • Mostly sucking insects are subjected to resurgence
• Their short life cycle
• Migrating ability
• Increased productivity and sensitiveness to the slight
change in food and environment. 70

71. Crop Pests
Resurgence causing
pesticides
Rice Brown planthopper (BPH) Perthane, endosulfan,
acephate, phosphamidon,
methomyl, cypermethrin,
triazophos, decamethrin,
diazinon, fenthion.
Cotton Whiteflies DDT,triazophos, phosalone,
synthetic pyrethroids like
cypermethrin, decamethrin,
fenvalerate
Sugarcane Pyrilla, whitefly High level of nitrogenous
fertilizers.
Vegetables
Chilli Yellowmite synthetic pyrethroids
Lady’s finger Aphid Disulfotan, phorate,
dimethoate
Brinjal Fruit borer Acephate
Muskmelon, watermelon Spidermite Ethion
Pests, pesticides and resurgence in Indian context
(Jayaraj, 1987)
71

72. Causes of pest resurgence:
Suppression of natural enemies:
• Insecticides, in general, exert adverse effects
on the parasites and predators of crop pests
and in many instances, this is considered as a
major causes for insect pest resurgence to
unmanageable proportions.
• Natural enemy mortality following broad
spectrum insecticide application suggested as a
important factor for BPH resurgence in rice
(Miyashita, 1963) 72

73. Factors influencing pesticide – induced resurgence of insect pests
73

74. Pest Resurgence
Pest (8)
Natural Enemy
74

75. Pest
Natural Enemy 75

76. pest
pest
76

77. Pest Resurgence
Note: 14 pests/leaf
77

78. Four processes contribute to resurgence
1. Reduced Biological Control (Secondary) – most
common with insects
2. Reduced Competition – most common with weeds
(mono vs. dicots)
3. Direct Stimulation of Pest – usually due to sub-
acute doses
4. Improved Crop Growth 78

79. Factors inducing resurgence
Reduction in Natural Enemy Populations
 Direct effects
 Indirect effects
 Hormoligosis
 Alteration of plant quality
 Induction of insect detoxification enzymes by plant secondary
chemicals and/or insecticides
 Direct and indirect enhancement of fecundity
 Effects of insecticide exposure on insect behaviour
 Reduction of competition
79

80. Preventing/Avoiding Pest Resurgence
 Avoiding hormoligosis
 Avoiding natural enemy destruction
 Avoiding competitor destruction
 Use physiologically selective control measures
 Use ecologically selective control measures
 Inoculative release of natural enemies
 Diversification of control methods
80

81. Thank You !!
81