insecticides and vector control Flashcards
1
Q
early insecticides
A
- non-selective → kill msot organisms in environment
- difficult to mass produce
- e.g. nicotine form tobacco plants
- used to derive modern insecticide classes
2
Q
modern insecticides
A
- neuroactive, synthetic compounds
- act as contact poisons
- organochlorides, organophosphates, carbamates, pyrethroids used for vector control
- neonicotinoids used in agriculture
3
Q
DDT
A
- used to eliminate malaria in europe (1975) by mass spraying
- toxic to wide insect range but not vertebrates
- persists in environment → no need to reapply
- water insoluble → not washed away by rain
- inexpensive
- banned in 1973 from agriculture
- limited use in malaria control now
4
Q
DDT resistance
A
- rapidly spread
- 20 years for A. albimanus in Guatemala to go from 0 to 100% resistance
- failure of vector control
- number of cases in sri lanka from 20 to what they were before treatment
- also accumulation in animal fat
5
Q
biomagnification
A
- DDT accumulation in animal/human fat, even far fromt reatment areas
- doesn’t dissolve in water but does in fat
- accumulates up food chain
- increased concentration
- little lost through excretion
- correlation to breast cancer
6
Q
organochlorides
A
- DDT, cyclodienes
- long persistence in environment
7
Q
pyrethroids
A
- permethrin, deltamethrin
- derived from pyrethrin of chrysanthemum
8
Q
carbamates
A
- propoxur, bendiocarb
- shorter persistence in evironment
- low mammalian toxicity
- characteristic carbamate group
9
Q
organophosphates
A
- temephos, malathione
- most toxic pesticide to vertebrates
- developed for military purposes
- relatively quick environmental breakdown
10
Q
action potentials
A
- travel across axon via localised depolarisation
- sodium ion influx → positive inside
- potassium efflux reestablishes resting potential
- mediated by voltage gated sodium channels
- open upon neighbouring depolarisation
- flaps attracted to other side of membrane
- reaches synapse
- calcium influx, neurotransmitter fusion and release
- neurotransmitter binds postsynaptic receptors creating AP
- neurotransmitter degraded and recycled
11
Q
insecticide action on nervous system
A
- organophosphates/carbamates
- directly block ACh recycling by AChE
- pyrethroids/DDT
- bind voltage gated sodium channels to alter function
- neonicotinoids
- bind ACh receptors
12
Q
sodium channel interference
A
- poorly established where and how binding occurs
- normally there is a refractory period after an AP has passed through
- insecticides allow opening and closing multiple times
- prevent closing
- sustained nerve stimulation
- uncoordinated movement
13
Q
AChE inactivation
A
- normally uses active site serine to attack ACh bond
- acetic acid release by water molecule coordination
- enzyme returns to ground state
- carbamates
- enter and block active site for hours
- organophosphates
- enter, phosphorylate serine and inactivate for days
- neither removed by water (much mroe stable)
- sustained nerve impulse firing across synapses
- uncontrolled movement
14
Q
selective toxicity of insecticides
A
- insects smaller
- less able to breakdown before target reached
- lower body temperature
- slower degradation
- increased potency (unsure why)
- different degradation enzymes
- often higher affinity for insect AChE
- partially redundant genes used by mammals
- sodium channel isoforms of varying sensitivity
- many toxic to vertebrates at higher dose
15
Q
neonicotinoids
A
- first new class in 30 years
- expensive
- resembles nicotine which resembles ACh
- binds ACh receptors → hyperstimulation → paralysis
- potentially declining honey bees
- slow withdrawal form europe
- much higher affinity for insect ACh receptor compared to mammalian
- coordinating side chain group not present in mammals
16
Q
other insecticide targets
A
- inhibitory neurons
- GABA receptors
- GluRs
- respiratory targets
- midgut targets
- growth/development inhibitors
- juvenile hormone analogues
- moutling disruptors
17
Q
inhibitory neuron targets
A
- fipronil
- blocks GABA receptors in CNS (gated chloride channels)
- 50x higher afifnity for insect form
- prevents inhibitory effect of Cl uptake → hyperstimulation
- avermectine
- irreversible opening of glutamate gated chloride channels (GluRs)
- excess Cl uptake → paralysis
- no GluRs in mammals
18
Q
respiration targets
A
- mitochondrial inhibitors
- uncouplers of oxidative phopshorylation
- inhibitors of acetyl CoA carboxylase
19
Q
midgut targets
A
- disrupt midgut membranes
- BT toxin
- expressed in transgenic crops
- ingested by insect → binds gut membrane receptor
- inserted into membrane leaving open channel
- ion flow through channel disturbing electrolyte balance
20
Q
onchocerca
A
- filarial nematode worm
- lives under skin → river blindness and dermatitis
- transmitted by black flies
- larvae in fast flowing rivers
- inflammation caused by Wolbachia endosymbiont of worm, not worm itself
21
Q
onchocerciasis control
A
- 1974 programme launched
- aerial insecticide spraying over breeding sites in west africa
- organophosphates
- BT toxins
- both aimed at larvae
- later ivermectin added to target worm
- 14 years
- elimination in most countries
- eventual cost <$1 per year per infected individual
22
Q
malaria control
A
- global eradication programme abandoned
- DDT banned
- 2-3 fold increase in cases 80s-90s
- Roll Back Malaria campaign launched 1998
- causes reduced 30%
- ITNs, IRS
- rapid diagnostic testing
- artemisinin
- larvae breed everywhere → difficult to target
- problems are insecticide resistance and lack of funding
23
Q
IRS
A
- indoor residual spraying
- spray on walls where mosquitoes feed and rest
- lasts but requires compliance
- widely used
- pyrethroids and carbamates
24
Q
ITNs
A
- insecticide treated bed nets
- reduces biting but can be bitten through
- baited trap to attract mosquito and kill them
- only pyrethroids stable enough
- reduces malaria in neighbouring control villages where ITNs not used
- not enough on its own
