Tick Resistance and Genetic Mechanisms

152 Questions

What is the term for changes in behavior that contribute to resistance?

Behavioral resistance

What type of genetic variation can confer resistance by altering the structure of target proteins?

Single Nucleotide Polymorphisms (SNPs)

What is the result of amplification of genes encoding detoxifying enzymes?

Enhanced metabolism of acaricides

What drives the increase in frequency of resistant alleles in a population?

Selection pressure

What facilitates the spread of resistant ticks and their genes?

Movement of livestock and wildlife

What type of diagnostic technique detects specific resistance-associated mutations?

Molecular diagnostics

What is the purpose of molecular diagnostics in monitoring resistance?

To detect low-frequency resistant alleles in tick populations

What is used to assess the susceptibility of ticks to acaricides?

Bioassays

What is the primary purpose of understanding genetic resistance in ticks?

To develop effective management strategies for controlling tick populations

What is the result of genetic changes in the genome of ticks?

Development of multiple defense mechanisms against acaricides

Which mechanism of genetic resistance involves the alteration of binding sites on target proteins?

Target Site Modifications

What is the role of enzymes like cytochrome P450 monooxygenases in genetic resistance?

To break down acaricides

What is the effect of genetic mutations on the sodium channel gene?

Confer resistance to pyrethroids

What is the result of changes in the tick's cuticle?

Reduced penetration of acaricides

What is the primary mechanism of genetic resistance that involves the upregulation of enzymes?

Metabolic Resistance

What is the ultimate goal of understanding genetic resistance in ticks?

To control tick populations

What is the main advantage of bioassays in detecting resistance levels in field populations?

They provide phenotypic data on resistance levels

What is the purpose of rotating acaricides with different modes of action?

To reduce the development of resistance

What is an example of biological control mentioned in the text?

Using fungal pathogens to control tick populations

What is the goal of genetic research and breeding in tick control?

To reduce the need for chemical interventions

What is the mechanism of pyrethroid resistance in the cattle tick?

A mutation in the voltage-gated sodium channel gene

What is the name of the mutation that confers pyrethroid resistance in the cattle tick?

kdr mutation

In which regions have pyrethroid-resistant Rhipicephalus microplus populations been found?

South America, India, and Australia

What is the main advantage of using genetic research and breeding in tick control?

It reduces the need for chemical interventions

What is the mechanism of organophosphate resistance in Rhipicephalus microplus?

Increased activity of carboxylesterase and glutathione S-transferase enzymes

Where has amitraz resistance been observed in Rhipicephalus sanguineus?

Southern Europe and the United States

What is the mechanism of amitraz resistance in Rhipicephalus sanguineus?

Mutations in octopamine receptors

What is the mechanism of avermectin resistance in Rhipicephalus microplus?

Amplification of the gene encoding P-glycoprotein

Where has avermectin resistance been discovered in Rhipicephalus microplus?

Brazil and Mexico

What is the effect of the mechanism of organophosphate resistance in Rhipicephalus microplus?

Reduced effectiveness of organophosphates

What is the primary mechanism of resistance to bromophos in the American dog tick?

Increased production of cytochrome P450 enzymes

What is the significance of understanding genetic resistance in ticks?

To improve the effectiveness of pest management strategies

What is the consequence of genetic resistance in ticks?

Reduced effectiveness of pest management strategies

What is the role of genetic research in mitigating the impact of tick resistance?

To develop effective management strategies integrating chemical and non-chemical methods

What is the importance of integrating chemical and non-chemical methods in pest management?

To mitigate the impact of tick resistance

What is the goal of developing effective management strategies for tick resistance?

To mitigate the impact of tick resistance on pest management

Ticks develop resistance through genetic mutations in binding sites of acaricides on target proteins.

True

Metabolic resistance involves downregulation of enzymes that break down acaricides.

False

Reduced penetration is a mechanism of genetic resistance that works independently of other mechanisms.

False

Understanding genetic resistance is essential for developing ineffective management strategies.

False

Genetic resistance leads to the development of a single defense mechanism against acaricides.

False

Ticks can develop resistance through genetic changes that occur in the genome.

True

Acaricides are effective against ticks that have developed genetic resistance.

False

Genetic resistance is the ability of ticks to be affected by acaricides.

False

Bioassays are more precise than molecular methods in detecting resistance trends.

False

Rotating acaricides with different modes of action can prevent the development of resistance.

False

Fungal pathogens like Metarhizium anisopliae and Beauveria bassiana have shown promise in controlling tick populations and contributing to resistance.

False

Breeding tick-resistant livestock is not a promising strategy in controlling tick populations.

False

The kdr mutation prevents pyrethroids from binding effectively to potassium channels.

False

Pyrethroid resistance in cattle tick is caused by a mutation in the gene encoding the acetylcholinesterase enzyme.

False

The primary purpose of understanding genetic resistance in ticks is to develop new acaricides.

False

Genetic research and breeding are not effective in controlling tick populations.

False

Behavioral resistance is a minor contributor to overall resistance patterns.

False

Avermectin resistance in Rhipicephalus microplus is due to mutations in octopamine receptors in nerve cells.

False

SNPs are associated with resistance to organophosphates.

False

Organophosphate resistance in Rhipicephalus microplus has been reported in populations in Southern Europe.

False

Gene amplification results in decreased production of detoxifying enzymes.

False

Continuous exposure to acaricides creates weak selection pressure.

False

Amitraz resistance in Rhipicephalus sanguineus is due to the amplification of the gene encoding P-glycoprotein.

False

Organophosphate resistance in Rhipicephalus microplus is due to the amplification of the gene encoding P-glycoprotein.

False

Molecular diagnostics are used to assess the susceptibility of ticks to acaricides.

False

Avermectin resistance in Rhipicephalus microplus has been discovered in populations in the United States.

False

Gene flow occurs through the movement of livestock and wildlife.

True

Bioassays are highly sensitive and can identify low-frequency resistant alleles in tick populations.

False

Amitraz resistance in Rhipicephalus sanguineus has been observed in populations in Brazil and Mexico.

False

The ultimate goal of understanding genetic resistance in ticks is to develop more effective acaricides.

False

Bromophos resistance in American dog ticks is due to a reduction in cytochrome P450 enzymes.

False

Genetic resistance in ticks is not a significant challenge to effective pest management.

False

Acaricides are a type of non-chemical method used in pest management.

False

The primary purpose of molecular diagnostics is to detect specific resistance-associated mutations.

True

The ultimate goal of understanding genetic resistance in ticks is to develop more effective acaricides.

False

Genetic research and breeding are not used in tick control.

False

Single Nucleotide Polymorphisms can confer resistance by altering the binding sites on target proteins.

False

Gene amplification results in decreased production of detoxifying enzymes.

False

Continuous exposure to acaricides reduces the frequency of resistant alleles in a population.

False

Molecular diagnostics can only detect high-frequency resistant alleles in tick populations.

False

Bioassays are used to detect specific resistance-associated mutations.

False

Behavioral resistance is not crucial for understanding overall resistance patterns.

False

Gene flow can introduce susceptible alleles into new populations, simplifying control efforts.

False

Molecular diagnostics are essential for guiding management practices, but not for monitoring resistance.

False

Ticks can develop resistance through genetic changes that occur in the environment.

False

Genetic resistance is the ability of ticks to be affected by acaricides.

False

Target site modifications involve upregulation of enzymes that break down acaricides.

False

Reduced penetration is a mechanism of genetic resistance that works independently of other mechanisms.

False

Acaricides are effective against ticks that have developed genetic resistance.

False

Metabolic resistance involves downregulation of enzymes that break down acaricides.

False

Genetic resistance leads to the development of multiple defense mechanisms against acaricides.

True

Understanding genetic resistance is essential for developing ineffective management strategies.

False

Carboxylesterase and glutathione S-transferase enzymes break down organophosphates before they affect the tick's nervous system.

True

Mutations in octopamine receptors in nerve cells increase the effectiveness of amitraz on these receptors.

False

P-glycoprotein reduces the concentration of avermectin within the tick's body.

True

Bioassays are more precise than molecular methods in detecting resistance trends.

False

Fungal pathogens like Metarhizium anisopliae and Beauveria bassiana contribute to resistance in controlling tick populations.

False

Organophosphate resistance has been reported in Rhipicephalus microplus populations in Africa.

False

Breeding tick-resistant livestock is not a promising strategy in controlling tick populations.

False

Amitraz resistance has been observed in Rhipicephalus sanguineus populations in North America.

False

The kdr mutation prevents pyrethroids from binding effectively to potassium channels.

False

Avermectin resistance has been discovered in Rhipicephalus microplus populations in Europe.

False

Rotating acaricides with different modes of action can prevent the development of resistance.

True

Genetic resistance is the ability of ticks to be affected by acaricides.

False

Ticks develop resistance through genetic mutations in binding sites of acaricides on target proteins.

True

Acaricides are effective against ticks that have developed genetic resistance.

False

In the American dog tick, increased production of cytochrome P450 enzymes metabolizes bromophos, increasing its toxic effects on the tick.

False

Genetic resistance in ticks presents a significant advantage to effective pest management.

False

Integrating chemical and non-chemical methods can help mitigate the impact of tick resistance.

True

Acaricides are ineffective against ticks that have developed genetic resistance.

True

Understanding genetic resistance is essential for developing ineffective management strategies for tick resistance.

False

Rotating acaricides with different modes of action can prevent the development of genetic resistance in ticks.

True

Fossil records show that the terrestrial Arachnida acquired respiratory organs of the same type during the transition from the marine environment onto land.

False

The Acari had achieved a certain amount of diversity by the late Silurian period.

False

In the early Devonian, all fossil Acari now known belonged to the superorder Parasitiformes.

False

The fossil records of the Parasitiformes date to the early Devonian.

False

Mesostigmatid mites have stigmata above the coxae of the first pair of legs.

False

The parasitiform Trigynaspida may date to as early as the upper Jurassic.

False

Studies of mitochondrial phylogeny have shown that the orders and classes of spiders, scorpions, mites, and ticks diversified in the early Palaeozoic.

False

Entonyssus, Entophionyssus, and Mabuyonysus are parasites of rodents.

False

Most species of Mesostigmata are ectoparasites of birds and mammals.

False

All Macronyssid mites are host-specific.

False

Sternosoma occurs only in domestic birds.

False

The protonymph and adult stages of Macronyssid mites do not feed.

False

The genus Linguatula is of some veterinary significance in dogs.

True

Dermanyssid mites are found in the respiratory tracts of mammals.

False

Pentastomids are up to 1.0 cm long.

False

Halarachnid mites are found in the ears of domestic cattle.

False

The oldest mite fossil is from the Cambrian period.

False

Entonyssid mites are found in the respiratory tract of mammals.

False

The advent of the Acari probably relates to the early part of the evolution of the arthropods.

False

Mesostigmatid mites are generally small.

False

The class Pentastomida is a group of arthropods that resemble annelid worms.

True

Androlaelaps, the poultry litter mite, is a parasite of wild birds.

False

Mesostigmatid mites are generally small, with multiple small shields on the dorsal surface.

False

The majority of Mesostigmatid mites are ectoparasites of birds and mammals.

False

The Macronyssidae and Dermanyssidae are two minor families of veterinary interest.

False

Only the deutonymph and adult stages of Macronyssidae feed.

False

Members of the subfamily Halarachinae are found in the nasal sinuses and nasal passages of dogs.

False

Raillietia is found in the ears of domestic cattle.

True

Mites of the family Entonyssidae are found in the respiratory tract of mammals.

False

The legs of Mesostigmatid mites are short and positioned posteriorly.

False

Androlaelaps, the poultry litter mite, is a parasite of rodents.

False

The terrestrial Arachnida acquired respiratory organs of the same type during the transition from the marine environment onto land.

False

Pentastomids are found in the respiratory passages of vertebrates and resemble arachnids.

False

The genus Linguatula is of some veterinary significance and occurs in the nasal passages and sinuses of dogs, cats, and foxes.

True

The fossil records indicate that the Acari had achieved a certain amount of diversity by the late Devonian.

False

The oldest mite fossil is from the Cambrian period.

False

The superorder Acariformes dates to the late Cretaceous.

False

The family Rhinonyssidae consists of parasites of birds' nasopharynxes.

True

The order Trigynaspida dates to the upper Triassic.

True

The class Pentastomida is a group of annelid worms.

False

The orders and classes of spiders, scorpions, mites, and ticks diversified in the early Palaeozoic.

False

The genus Sternosoma occurs worldwide in various domestic and wild birds.

True

The terrestrial Acari colonized terrestrial environments as early as the late Devonian.

False

The family Laelapidae consists of blood-feeding parasites of snakes.

False

Study Notes

Genetic Resistance in Ticks

Ticks are significant ectoparasites affecting both animals and humans by transmitting various pathogens.
Genetic resistance is the ability of organisms to withstand or survive the harmful effects of environmental or chemical agents due to genetic changes.
Ticks develop resistance through several genetic mechanisms:

Mechanisms of Genetic Resistance

Target Site Modifications: Genetic mutations alter the binding sites of acaricides on target proteins, reducing the efficacy of the chemicals.
Metabolic Resistance: Enhanced detoxification involves upregulation of enzymes like cytochrome P450 monooxygenases, esterases, and glutathione S-transferases, which break down acaricides.
Reduced Penetration: Changes in the tick's cuticle can reduce the penetration of acaricides, limiting the amount of the chemical that reaches internal tissues.
Behavioral Resistance: Changes in behavior, such as reduced time spent on treated surfaces or avoidance of treated animals, also contribute to resistance.

Genetic Basis of Resistance

Single Nucleotide Polymorphisms (SNPs): SNPs are common genetic variations that confer resistance by altering the structure of target proteins.
Gene Amplification: Amplification of genes encoding detoxifying enzymes results in increased production of these enzymes, enhancing the tick's ability to metabolize acaricides.

Evolution and Spread of Resistance

Selection Pressure: Continuous exposure to acaricides creates strong selection pressure, favoring resistant individuals.
Gene Flow: Movement of livestock and wildlife facilitates the spread of resistant ticks and their genes, introducing resistant alleles into new populations.

Diagnostic and Management Approaches

Molecular Diagnostics: Techniques like PCR and qPCR detect specific resistance-associated mutations.
Bioassays: Bioassays involve exposing ticks to various concentrations of acaricides to assess their susceptibility.

Integrated Management Strategies

Rotation of Acaricides: Rotating acaricides with different modes of action can prevent or delay the development of resistance.
Biological Control: Utilizing natural predators, parasitoids, and pathogens to control tick populations can reduce reliance on chemical acaricides.
Genetic Research and Breeding: Advances in genetic research, such as genome sequencing and gene editing, can lead to new control methods. Breeding tick-resistant livestock is another promising strategy.

Examples of Genetic Resistance in Ticks

Pyrethroid Resistance in Cattle Tick (Rhipicephalus microplus): Mutation in the voltage-gated sodium channel gene, known as the kdr (knockdown resistance) mutation.
Organophosphate Resistance in Cattle Tick (Rhipicephalus microplus): Increased activity of carboxylesterase and glutathione S-transferase enzymes.
Amitraz Resistance in Brown Dog Tick (Rhipicephalus sanguineus): Mutations in octopamine receptors in nerve cells.
Avermectin Resistance in Cattle Tick (Rhipicephalus microplus): Amplification of the gene encoding P-glycoprotein.
Bromophos Resistance in American Dog Tick (Dermacentor variabilis): Increased production of cytochrome P450 enzymes.

Genetic Resistance in Ticks

Ticks are significant ectoparasites affecting both animals and humans by transmitting various pathogens.
Genetic resistance is the ability of organisms to withstand or survive the harmful effects of environmental or chemical agents due to genetic changes.
Ticks develop resistance through several genetic mechanisms:

Mechanisms of Genetic Resistance

Target Site Modifications: Genetic mutations alter the binding sites of acaricides on target proteins, reducing the efficacy of the chemicals.
Metabolic Resistance: Enhanced detoxification involves upregulation of enzymes like cytochrome P450 monooxygenases, esterases, and glutathione S-transferases, which break down acaricides.
Reduced Penetration: Changes in the tick's cuticle can reduce the penetration of acaricides, limiting the amount of the chemical that reaches internal tissues.
Behavioral Resistance: Changes in behavior, such as reduced time spent on treated surfaces or avoidance of treated animals, also contribute to resistance.

Genetic Basis of Resistance

Single Nucleotide Polymorphisms (SNPs): SNPs are common genetic variations that confer resistance by altering the structure of target proteins.
Gene Amplification: Amplification of genes encoding detoxifying enzymes results in increased production of these enzymes, enhancing the tick's ability to metabolize acaricides.

Evolution and Spread of Resistance

Selection Pressure: Continuous exposure to acaricides creates strong selection pressure, favoring resistant individuals.
Gene Flow: Movement of livestock and wildlife facilitates the spread of resistant ticks and their genes, introducing resistant alleles into new populations.

Diagnostic and Management Approaches

Molecular Diagnostics: Techniques like PCR and qPCR detect specific resistance-associated mutations.
Bioassays: Bioassays involve exposing ticks to various concentrations of acaricides to assess their susceptibility.

Integrated Management Strategies

Rotation of Acaricides: Rotating acaricides with different modes of action can prevent or delay the development of resistance.
Biological Control: Utilizing natural predators, parasitoids, and pathogens to control tick populations can reduce reliance on chemical acaricides.
Genetic Research and Breeding: Advances in genetic research, such as genome sequencing and gene editing, can lead to new control methods. Breeding tick-resistant livestock is another promising strategy.

Examples of Genetic Resistance in Ticks

Pyrethroid Resistance in Cattle Tick (Rhipicephalus microplus): Mutation in the voltage-gated sodium channel gene, known as the kdr (knockdown resistance) mutation.
Organophosphate Resistance in Cattle Tick (Rhipicephalus microplus): Increased activity of carboxylesterase and glutathione S-transferase enzymes.
Amitraz Resistance in Brown Dog Tick (Rhipicephalus sanguineus): Mutations in octopamine receptors in nerve cells.
Avermectin Resistance in Cattle Tick (Rhipicephalus microplus): Amplification of the gene encoding P-glycoprotein.
Bromophos Resistance in American Dog Tick (Dermacentor variabilis): Increased production of cytochrome P450 enzymes.

Genetic Resistance in Ticks

Ticks are significant ectoparasites affecting both animals and humans by transmitting various pathogens.
Genetic resistance is the ability of organisms to withstand or survive the harmful effects of environmental or chemical agents due to genetic changes.
Ticks develop resistance through several genetic mechanisms:

Mechanisms of Genetic Resistance

Target Site Modifications: Genetic mutations alter the binding sites of acaricides on target proteins, reducing the efficacy of the chemicals.
Metabolic Resistance: Enhanced detoxification involves upregulation of enzymes like cytochrome P450 monooxygenases, esterases, and glutathione S-transferases, which break down acaricides.
Reduced Penetration: Changes in the tick's cuticle can reduce the penetration of acaricides, limiting the amount of the chemical that reaches internal tissues.
Behavioral Resistance: Changes in behavior, such as reduced time spent on treated surfaces or avoidance of treated animals, also contribute to resistance.

Genetic Basis of Resistance

Single Nucleotide Polymorphisms (SNPs): SNPs are common genetic variations that confer resistance by altering the structure of target proteins.
Gene Amplification: Amplification of genes encoding detoxifying enzymes results in increased production of these enzymes, enhancing the tick's ability to metabolize acaricides.

Evolution and Spread of Resistance

Selection Pressure: Continuous exposure to acaricides creates strong selection pressure, favoring resistant individuals.
Gene Flow: Movement of livestock and wildlife facilitates the spread of resistant ticks and their genes, introducing resistant alleles into new populations.

Diagnostic and Management Approaches

Molecular Diagnostics: Techniques like PCR and qPCR detect specific resistance-associated mutations.
Bioassays: Bioassays involve exposing ticks to various concentrations of acaricides to assess their susceptibility.

Integrated Management Strategies

Rotation of Acaricides: Rotating acaricides with different modes of action can prevent or delay the development of resistance.
Biological Control: Utilizing natural predators, parasitoids, and pathogens to control tick populations can reduce reliance on chemical acaricides.
Genetic Research and Breeding: Advances in genetic research, such as genome sequencing and gene editing, can lead to new control methods. Breeding tick-resistant livestock is another promising strategy.

Examples of Genetic Resistance in Ticks

Pyrethroid Resistance in Cattle Tick (Rhipicephalus microplus): Mutation in the voltage-gated sodium channel gene, known as the kdr (knockdown resistance) mutation.
Organophosphate Resistance in Cattle Tick (Rhipicephalus microplus): Increased activity of carboxylesterase and glutathione S-transferase enzymes.
Amitraz Resistance in Brown Dog Tick (Rhipicephalus sanguineus): Mutations in octopamine receptors in nerve cells.
Avermectin Resistance in Cattle Tick (Rhipicephalus microplus): Amplification of the gene encoding P-glycoprotein.
Bromophos Resistance in American Dog Tick (Dermacentor variabilis): Increased production of cytochrome P450 enzymes.

Mesostigmata

A large group of mites, mostly predatory, but some species are ectoparasites of birds and mammals
Stigmata are located above the coxae of the second, third, or fourth pairs of legs
Typically large, with one large sclerotized shield on the dorsal surface and a series of smaller shields in the midline of the ventral surface
Legs are long and positioned anteriorly

Families of Mesostigmata

Macronyssidae: relatively large, blood-sucking ectoparasites of birds and mammals (e.g. Ornithonyssus, Ophionyssus)
Dermanyssidae: blood-feeding ectoparasites of birds and mammals (e.g. Dermanyssus)
Halarachinidae: mites found in mammals' respiratory tracts (e.g. Pneumonyssus)
Entonyssidae: mites found in the respiratory tract of reptiles (e.g. Entonyssus, Entophionyssus, Mabuyonysus)
Rhinonyssidae: mites found in birds' nasopharynxes (e.g. Sternosoma)
Laelapidae: blood-feeding parasites of rodents (e.g. Hirstionyssus, Haemogamasus, Haemolaelaps, Echinolaelaps, Eulaelaps, Laelaps)

Class Pentastomida

A strange class of aberrant arthropods
Adults are found in the respiratory passages of vertebrates
Resemble annelid worms rather than arthropods
Genus Linguatula is of some veterinary significance (e.g. adult parasites in the nasal passages and sinuses of dogs, cats, and foxes)

Fossil Records of Acari

First fossil records date back to the late Silurian-early Devonian periods (c.425 mya)
Oldest mite fossil is from the Devonian (410 mya)
Fossil records show that the Acari had achieved a certain amount of diversity by the early to mid-Devonian
Terrestrial Arachnida acquired respiratory organs of different types at different times during the transition from the marine environment onto land

Mesostigmata

A large group of mites, mostly predatory, but some species are ectoparasites of birds and mammals
Stigmata are located above the coxae of the second, third, or fourth pairs of legs
Typically large, with one large sclerotized shield on the dorsal surface and a series of smaller shields in the midline of the ventral surface
Legs are long and positioned anteriorly

Families of Mesostigmata

Macronyssidae: relatively large, blood-sucking ectoparasites of birds and mammals (e.g. Ornithonyssus, Ophionyssus)
Dermanyssidae: blood-feeding ectoparasites of birds and mammals (e.g. Dermanyssus)
Halarachinidae: mites found in mammals' respiratory tracts (e.g. Pneumonyssus)
Entonyssidae: mites found in the respiratory tract of reptiles (e.g. Entonyssus, Entophionyssus, Mabuyonysus)
Rhinonyssidae: mites found in birds' nasopharynxes (e.g. Sternosoma)
Laelapidae: blood-feeding parasites of rodents (e.g. Hirstionyssus, Haemogamasus, Haemolaelaps, Echinolaelaps, Eulaelaps, Laelaps)

Class Pentastomida

A strange class of aberrant arthropods
Adults are found in the respiratory passages of vertebrates
Resemble annelid worms rather than arthropods
Genus Linguatula is of some veterinary significance (e.g. adult parasites in the nasal passages and sinuses of dogs, cats, and foxes)

Fossil Records of Acari

First fossil records date back to the late Silurian-early Devonian periods (c.425 mya)
Oldest mite fossil is from the Devonian (410 mya)
Fossil records show that the Acari had achieved a certain amount of diversity by the early to mid-Devonian
Terrestrial Arachnida acquired respiratory organs of different types at different times during the transition from the marine environment onto land

Learn about the importance of controlling tick populations and the challenges of genetic resistance to acaricides. Understand the mechanisms behind genetic resistance and its impact on developing effective management strategies.

Make Your Own Quizzes and Flashcards

Convert your notes into interactive study material.