**1. Introduction**

Insects, ticks, and mites are the main groups of arthropods, including species that can be pests and disease vectors. Historically, the problem with arthropod pests and disease vectors affecting public health, crop yields, and livestock production has been managed through the

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massive use of pesticides. The widespread use of pesticides exerted strong selective pressure and now several of the most economically important arthropod species are resistant to currently used pesticides.

Pesticide resistance in arthropod species of public health, agricultural, and veterinary impor‐ tance has become a major problem. This situation presents a threat for societies around the world because several arthropod species attack crops and thus compete directly for food with humans, and other species are important vectors of infectious agents causing diseases in humans, livestock, wildlife, and plants [1]. The origin of resistance arises through evolutionary genetic changes, causing modifications in the molecular structure of the target site or promot‐ ing changes in multigenic metabolizing enzyme systems, resulting in high hydrolysis rates or sequestration of pesticides as well as a reduced capability to penetrate the outer chitin protective layer.

Here we review the known molecular and biochemical mechanisms of pesticide resistance and do a gap analysis of processes involved in the evolution of insensitivity to pesticides among arthropods that remain to be fully understood. Significant advances have been achieved in our knowledge of the processes involved in resistance to pyrethroids. More research is required to decrease the knowledge gaps regarding mechanisms of resistance to organophosphates (OP). Less is still known about resistance to amitraz, macrocyclic lactones, and fipronil, whose mechanisms of action appear to involve complex and multifactorial evolutionary mechanisms.

An example of the problem with pesticide-resistant pests is the cattle tick *Rhipicephalus (Boophilus) microplus*, which is regarded as the most economically important ectoparasite of livestock globally and ranks sixth among the most pesticide resistant pests globally. This cattle tick affects animal health and production in tropical and subtropical regions of the world directly through its obligate hematophagous habit and indirectly by serving as vector of pathogens like *Babesia bovis*, *B*. *bigemina* and *Anaplasma marginale*, which cause the deadly bovine diseases babesiosis and anaplasmosis, [1, 2]. The control of cattle ticks, bovine babe‐ siosis and anaplasmosisis a costly problem that prevents the livestock industry in Latin America and other parts of the world achieving its full potential [1]. The almost complete reliance on pesticides to control cattle ticks and associated diseases has been a strong selective force for tick populations that now are resistant to multiple classes of acaricides [3]. These developments highlight the super genetic plasticity and exquisite adaptability of arthropod pests and vectors, which has enabled them to become resistant to most classes of synthetic pesticides humans have discovered and developed for commercialization.

## **2. Resistance, adaptation and coevolution**

Resistance to synthetic pesticides is a genetic condition that confers an arthropod population the capability to get adapted to a toxic environment through a selection process driven by human activity [4]. Based on this concept, the phenomenon of pesticide resistance can be understood as an important model based on natural selection processes [5]. Considering pesticide resistance as a biological model facilitates the study of evolutionary adaptations by arthropods living under selection pressure through constant exposure to pesticides used by humans [6]. However, the natural history of pest-host interactions in a way preadapted arthropods to become resistant to synthetic pesticides.

massive use of pesticides. The widespread use of pesticides exerted strong selective pressure and now several of the most economically important arthropod species are resistant to

Pesticide resistance in arthropod species of public health, agricultural, and veterinary impor‐ tance has become a major problem. This situation presents a threat for societies around the world because several arthropod species attack crops and thus compete directly for food with humans, and other species are important vectors of infectious agents causing diseases in humans, livestock, wildlife, and plants [1]. The origin of resistance arises through evolutionary genetic changes, causing modifications in the molecular structure of the target site or promot‐ ing changes in multigenic metabolizing enzyme systems, resulting in high hydrolysis rates or sequestration of pesticides as well as a reduced capability to penetrate the outer chitin

Here we review the known molecular and biochemical mechanisms of pesticide resistance and do a gap analysis of processes involved in the evolution of insensitivity to pesticides among arthropods that remain to be fully understood. Significant advances have been achieved in our knowledge of the processes involved in resistance to pyrethroids. More research is required to decrease the knowledge gaps regarding mechanisms of resistance to organophosphates (OP). Less is still known about resistance to amitraz, macrocyclic lactones, and fipronil, whose mechanisms of action appear to involve complex and multifactorial evolutionary mechanisms. An example of the problem with pesticide-resistant pests is the cattle tick *Rhipicephalus (Boophilus) microplus*, which is regarded as the most economically important ectoparasite of livestock globally and ranks sixth among the most pesticide resistant pests globally. This cattle tick affects animal health and production in tropical and subtropical regions of the world directly through its obligate hematophagous habit and indirectly by serving as vector of pathogens like *Babesia bovis*, *B*. *bigemina* and *Anaplasma marginale*, which cause the deadly bovine diseases babesiosis and anaplasmosis, [1, 2]. The control of cattle ticks, bovine babe‐ siosis and anaplasmosisis a costly problem that prevents the livestock industry in Latin America and other parts of the world achieving its full potential [1]. The almost complete reliance on pesticides to control cattle ticks and associated diseases has been a strong selective force for tick populations that now are resistant to multiple classes of acaricides [3]. These developments highlight the super genetic plasticity and exquisite adaptability of arthropod pests and vectors, which has enabled them to become resistant to most classes of synthetic

pesticides humans have discovered and developed for commercialization.

Resistance to synthetic pesticides is a genetic condition that confers an arthropod population the capability to get adapted to a toxic environment through a selection process driven by human activity [4]. Based on this concept, the phenomenon of pesticide resistance can be understood as an important model based on natural selection processes [5]. Considering pesticide resistance as a biological model facilitates the study of evolutionary adaptations by

**2. Resistance, adaptation and coevolution**

currently used pesticides.

336 Insecticides Resistance

protective layer.

As a naturally occurring process, the coevolution between plants and arthropods enabled biological and chemical interactions over hundreds of millions of years [7]. As a result of the interactions between these two groups of organisms [8], arthropod species conserved within their genomes genes conferring an evolutionary advantage, or traits that have allowed them to survive. These types of interactions called allelochemical interactions have allowed plants and arthropods to develop very sophisticated molecular mechanisms to maximize their chances of survival. Plants evolved to be a factory of potent allelochemicals such as natural poisons, toxins, and repellents that function as a natural mechanism of defense against predators. As an example of coevolution, herbivore arthropods adapted by evolving a machinery of metabolic hydrolyzing enzymes to prevent poisoning by allelochemicals acquired during plant feeding [9–11]. This resulted in what could be described as natural resistance in arthropods selected through exposure to plant allelochemicals, which took millions of years. Arthropods were in a way preadapted to become resistant to synthetic pesticides rapidly in terms of evolutionary time [12]. Another predisposing factor for this rapid adaptation is the structural analogy between secondary metabolites produced by plants and synthetic pesticides designed by humans to control pests [13, 14].

The development of resistance to chemicals depends on the evolutionary forces exerting selection pressure and the consequent adaptive processes involving selection of genetic variations caused by random mutations, or genetic rearrangements resulting from exposure to pesticides [7], which is reflected in the selection and reproduction of individuals with resistant phenotypes capable of surviving pesticide concentrations that are lethal to the wildtype populations.

Resistance occurs when the selection of low frequency naturally occurring mutations within the genetic pool of a population allows a small fraction of individuals to survive the toxic effect of compounds used as pesticides [15]. Prior to initial exposure of the population to pesticides, there are few individuals with resistant genotypes and most of them are susceptible. When a pesticide is applied, those few survivors have an adaptive advantage. Therefore, they survive initial exposure and reproduce, and the frequency of resistant genotypes in the progeny increases. If repetitive and sustained applications of the pesticide on the population occur, the susceptible individuals are eliminated, which drives the selection of resistant genotypes in the population. At this point, the diverse genetic traits conferring an advantage to survive pesticide exposure are transferred to the progeny and the efficacy of the pesticides decreases.
