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Benefits and Risks of Pesticide Usage in Pets

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Motunrayo Ganiyat Akande, Solomon Usman Abraham and Johnson Caleb Ogunnubi

Submitted: March 8th, 2022Reviewed: March 22nd, 2022Published: May 6th, 2022

DOI: 10.5772/intechopen.104630

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PesticidesEdited by Marcelo L. Larramendy

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Pesticides [Working Title]

Dr. Marcelo L. Larramendy and Dr. Sonia Soloneski

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Abstract

The purpose of this chapter was to highlight the advantages of applying pesticides for the optimum care of pet animals, while also outlining the adverse effects that may be associated with their use. Pesticides can be defined as substances that can be applied for the prevention, control or eradication of unwanted organisms in living systems or in the environment. Companion animals, fondly called “pets” include dogs, cats, ferrets, pet birds and some laboratory animals like albino rats, rabbits, guinea pigs, etc. Pesticides are usually applied on pets to control ectoparasites like ticks, fleas, mites, among others. However, pets may be poisoned by pesticides if their dosages and appropriate routes of administration are not strictly adhered to. Pesticides should be administered to pets by Veterinarians and other suitably qualified personnel. Subsequently, the pets should be monitored for signs of toxicity and be treated promptly if such develop.

Keywords

  • pesticides
  • pets
  • benefits
  • risks
  • toxicity
  • ectoparasites

1. Introduction

Pesticides are substances or mixtures of substances that possess unique chemical properties for the control of detrimental pests and insect vectors [1, 2]. Pests are living organisms that pose health risks such as biting and sucking, transmission of allergy-inducing constituents, diseases, as well as parasites, thereby causing harm to humans, animals and various components of the ecosystem [3]. Pesticides can be classified as algicides, insecticides, fungicides, herbicides, rodenticides, pyrethroids, fumigants, miticides, molluscicides, etc. with discrete chemical characteristics that decrease economic, health, and environmental risks elicited by pests [4, 5]. The inappropriate application of pesticides can evoke deleterious outcomes in several organisms and the environment. Notably, pesticides do not usually differentiate between pests and other living things, consequently they may cause injury to the organisms they encounter [1].

It has been observed that pesticides may gain access into biological systems through diverse routes. For instance, organophosphate and carbamate insecticides are quickly absorbed after dermal, oral, and inhalation exposures [6]. Damalas and Koutroubas [7] reported that pesticide applicators are commonly exposed to pesticides through the dermal route. Besides, pesticides may be absorbed dermally through a splash, spill, or spray device, when being mixed, loaded or disposed of [8]. Liquid preparations of pesticides are more readily absorbed through the dermal route and other body tissues compared to powders, dusts and granular types [7]. According to [8], oral exposure to a pesticide may occur by accident or intentionally. Moreover, marked damages to the nasal, throat and pulmonary tissues have been observed after inhalation of appreciable quantities of pesticides [7].

Furthermore, exposure of populations to pesticides have been associated with negative health conditions including cancers, congenital disorders, immunological aberrations, respiratory, neurobehavioral and reproductive deficits [9]. These undesirable effects of pesticides may be evoked in several tissues and organs through genetic impairments, epigenetic alterations, mitochondrial dysfunction, oxidative damage, endoplasmic reticulum stress, endocrine disruption, among others [10]. Some of the clinical manifestations of pesticide toxicosis are confusion, agitation, lacrimation, salivation, emesis, bronchospasm, respiratory failure, micturition, diarrhoea, muscle weakness, paralysis, fasciculations, etc. [11].

Pets are animals that are domesticated and catered for by human beings for companionship, pleasure, provision of services and assistance, among others. They include dogs, cats, ferrets, pet birds, rodents, rabbits, guinea pigs, as well as exotic species like cubs, reptiles, etc. Pets are an essential part of human lives and they have been existing with human beings for thousands of years [12]. They are continually exposed to fleas and ticks. These ectoparasites may cause distress, itching, anaemia and systemic infections in the pets [13]. It is crucial to control ectoparasites in companion animals to prevent vector-borne diseases that may eventually result in high morbidity and mortality [14]. Moreover, the presence of fleas and ticks on pets may make their owners vulnerable to parasitism and zoonosis [15, 16].

The purpose of this chapter was to highlight the advantages of using pesticides for the optimum care of pet animals, while also outlining the adverse effects that may be associated with their applications.

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2. Benefits of pesticide usage in pets

Insecticides such as organophosphates (e.g., malathion, diazinon, phosmet, fenthion, chlorfenvinphos, and cythioate) and carbamates (e.g., carbaryl and propoxur) are used to control insect and nematode infestations in animals [17]. They are formulated as sprays, pour-ons, baits, collars, etc. [17]. Carbamates are used more frequently because they are considered safer than organophosphates. However, some signs of intoxication linked to the application of carbamates are abdominal cramping, emesis, diarrhoea, dyspnoea, seizures, among others [18]. Organophosphate and carbamate insecticides competitively impede acetylcholinesterase by binding to its esteric site [19]. The excessive acetylcholine that ensues brings about unwarranted stimulation of smooth muscles and glandular secretions [17]. However, the inhibition of acetylcholinesterase by organophosphates is irreversible, while the inhibition by carbamates is reversible [20]. The classification, examples, routes of administration and mechanisms of toxicity of some insecticides applied to pets are shown in Table 1.

Classification of insecticidesExamplesMode of administrationMechanisms of toxicity
OrganophosphatesDiazinon, phosmet, cythioateSprays, pour-ons, collarsInhibition of acetylcholinesterase [19]
PyrethroidsCypermethrin, permethrinShampoos, dips, spot-ons and spraysInterruption of sodium channels in neurons [21, 22]
CarbamatesCarbaryl and propoxurSprays, pour-ons, collarsInhibition of acetylcholinesterase [19]
NeonicotinoidsImidacloprid, dinotefuran, nitenpyramImidacloprid and dinotefuran are applied as spot-on topical products. Nitenpyram is administered per os.Act as agonists on the postsynaptic acetylcholine receptors in insects [23, 24]
IsoxazolinesFluralaner, afoxolaner, sarolanerOral administrationBlockage of arthropod ligand-gated chloride channels [17]
Benzoylphenylurea derivativeLufenuronOral suspension and injectable preparation for cats. Oral tablets for dogs.Chitin (exoskeleton) synthesis inhibitor [25]
Insect growth regulatorsMethoprene, fenoxycarb, pyriproxyfenOral suspensions, sprays and spot-onsMimic insect hormones, thereby interfering with the growth and development of insects [26]
Oxadiazine insecticideIndoxacarbAdministered topically in a spot-on formulationBioactivation to an active metabolite that blocks the voltage-gated sodium ion conduits in insects [18]
Phenylpyrazole insecticideFipronilTopical administrationBinds to gamma-aminobutyric acid receptors and the glutamate-gated chloride channels in the central nervous systems of invertebrates [13, 27, 28, 29]
Macrocyclic lactonesSelamectin, aprinomectin, milbemycinTopical administrationBind to glutamate-gated chloride channels in the nervous systems of parasites [18]
FormamidinesAmitrazAvailable as a dip. Also formulated as impregnated collars for dogsBinds to octopamine receptors for its insecticidal effects [18]
SpinosynsSpinosadFormulated as edible tablets for dogs and catsTargets the binding sites on nicotinic acetylcholine receptors [18]

Table 1.

Classification, examples, route of administration and mechanisms of toxicity of some insecticides applied to pets.

Pyrethroids are synthetic derivatives of natural pyrethrins derived from the plant, Chrysanthemum cinerariaefolium, and they contain esters of chrysanthemum acid [21]. They are 2250 times more poisonous to insects compared to higher organisms [30]. This is because insects possess additional sensitive sodium channels, a reduced conformation and lower body temperature [30]. Permethrin, a type I pyrethroid, exists in the form of a liquid, yellow-brown and brown crystals, and it is soluble in organic solvents [31]. It may enter the body through the dermal, oral and inhalational routes [32, 33]. It is found in shampoos, dips, spot-ons, and sprays for the control of ectoparasites in companion animals [33]. Also, it is used for the treatment of scabies and lice [31, 34, 35]. Permethrin evokes injury to insect neurons by elevating the impulse conduction, thereby causing paralysis and death of insects [21]. It is broken down in the body by hydrolysis, esterification, oxidation and conjugation [30, 36].

Its metabolites include cis-3-(2,2 dichlorovinyl) 2,2 dimethylcyclopropane-1-carboxylic acid, trans-3-(2,2-dichlorovinyl)-2,2 dimethylcyclopropane-1-carboxylic acid) and (3 phenoxybenzoic acid) [31]. The metabolites of permethrin are principally excreted in the urine and faeces [21].

Furthermore, cypermethrin, a type II pyrethroid insecticide, is used for the control of pests in agricultural, public and animal health programmes [37]. It evokes toxicity through the interruption of sodium channels in neurons, thereby disrupting neuronal transmission [22]. Also, it produces oxidative stress in living organisms [38, 39, 40]. Type II pyrethroids are more neurotoxic relative to type I pyrethroids because of their α-cyano constituents [41].

Another class of insecticides administered for pest control in pets are neonicotinoid insecticides such as imidacloprid, nitenpyram and dinotefuran (stated in Table 1). Imidacloprid is structurally similar to nicotine, and is endorsed as a topical spot-on for dogs, as well as for agricultural purposes [14, 23]. It exerts its insecticidal activities by binding to the acetylcholine receptor on the postsynaptic region of insect neurons, thereby averting acetylcholine binding [23, 24]. Besides, imidacloprid has been reported to elicit oxidative stress and cause injury to crucial biological molecules such as deoxyribonucleic acid, proteins and lipids [42]. Moreover, nitenpyram is administered per os to eliminate fleas in dogs and cats [18]. It undergoes fast absorption with utmost blood concentrations attained within one and a half hours, and thirty-six minutes in dogs and cats respectively [18]. Dinotefuran is applied as a topical spot-on with different formulations for dogs and cats against external parasites like fleas, flies, lice, etc. [43].

Fluralaner (an isoxazoline) is a systemically administered insecticidal and acaricidal formulation that elicits long-acting efficacy after oral administration to dogs [44]. Another isooxazoline, afoxolaner, has been reported to be efficacious in dogs and cats against fleas [45, 46, 47], ticks [46], and mites [47, 48, 49, 50]. It is detected in plasma 20–30 minutes following administration through the oral route and it attains its uppermost level in 2–4 hours [51]. Sarolaner is a broad spectrum isooxazoline with efficacy against fleas, ticks and mites in dogs [52, 53]. Isoxazolines bind to the ligand-gated chloride channels in insects and acarines [17]. Consequently, the presynaptic and postsynaptic transmission of chloride ions across the cell membranes ensue, thereby causing hyperexcitation and uninhibited activity of the central nervous system, ultimately resulting in the death of ectoparasites [17].

Lufenuron, a benzoylphenylurea derivative, is a chitin synthesis inhibitor [25]. It is available as an oral suspension and injectable formulation for cats, and an oral tablet for dogs [17]. It eliminates emerging larvae within the egg or after hatching, and female fleas feeding on treated animals are hindered from producing viable eggs or larvae [25].

Methoprene is an insect growth regulator that mimics insect hormones, thereby interfering with the growth and development of insects [26]. It is formulated as suspensions, emulsifiable and soluble concentrates, sprays and spot-ons, etc. [17]. It is used for flea control in dogs and cats, marine mosquito control, as well as agricultural and domestic pest control [54].

Fipronil is a phenylpyrazole insecticide that is approved for agricultural usage, pest control, as well as topical flea and tick treatment for companion animals [55]. It dissolves in sebum because of its high lipid solubility and it is disseminated throughout the body for the manifestation of its insecticidal effect [13]. It has been shown that fipronil binds non-competitively to γ-aminobutyric acid (GABA) receptors and the glutamate-gated chloride channels in the central nervous systems of invertebrates (e.g., fleas and ticks), thereby eliciting excessive excitation [13]. Additionally, fipronil also binds to mammalian GABA receptors, [27], and engenders oxidative stress through the production of reactive oxygen species [28, 29]. Some investigators have asserted that the foremost metabolite of fipronil, fipronil sulfone, exerts a more robust inhibitory effect on GABAA receptors and brings about cell impairment at lesser concentrations compared to fipronil [27, 28, 29].

Selamectin, aprinomectin and milbemycin are macrocyclic lactones that are used for the control of endoparasites and ectoparasites in dogs and cats [18]. They are widely administered for the prevention of heartworm disease in dogs [56]. Selamectin and aprinomectin are semisynthetic avermectins, while moxidectin is semisynthetic. These substances bind to glutamate-gated chloride channels in the nervous systems of parasites, and this culminates in a speedy and sustained entry of chloride ions into neurons [18]. As a result of this, the activity of the neurons is impeded and paralysis of the parasites occurs. The macrocyclic lactones are administered topically, and are swiftly absorbed through the dermal route. Selamectin exhibits effective control against the flea, Ctenocephalides felis[57, 58], biting lice (Felicola subrostratus) and ear mites (Otodectes cynotis), among others in cats [59].

Indoxacarb is an oxadiazine insecticide that is administered topically in a spot-on formulation for the control of fleas on companion animals [18]. It is found in insect baits for home use and granules, as well as liquids for agricultural applications [60]. Moreover, it is bioactivated to an active metabolite that blocks the voltage-gated sodium ion conduits in insects [18].

Furthermore, formamidines are acaricidal compounds that exert their effects through binding to octopamine receptors [18]. Amitraz is the only approved formamidine for use in veterinary medical practice, and it is applied primarily as an acaricide to control ticks and mites [18]. It is available as a dip for the control of demodicosis in dogs, as well as the control of scabies. An amitraz-impregnated collar is also marketed for the control of ticks on dogs.

Spinosyns are a family of insecticides obtained from the fermentation of an actinomycete, Saccharopolyspora spinosa[18]. Spinosyns A and D are the main products of the fermentation procedure, as well as the principal components of Spinosad [61]. Spinosyns mostly target the binding sites on nicotinic acetylcholine receptors, and they also influence GABA receptor function [18]. This ensues in spontaneous muscle contractions, prostration, tremors, and paralysis of insects. Spinosad is used to control numerous insects and it is formulated as edible tablets for dogs and cats [61].

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3. Risks of pesticide usage in pets

There is a predominant exposure of human and animal populations to pesticides and this may be associated with detrimental effects on their health status [4, 62]. According to [17] , clinical signs of pesticide intoxication can occur within a short or long duration of exposure, depending on the dose, route, and noxiousness of the pesticide administered. It has been documented that those pesticides have severe effects on non-target organisms, including various components of the ecosystem [63].

Various pesticides, especially, insecticides applied to pets for the prevention and control of ectoparasites may be associated with some adverse effects. For instance, permethrin poisoning may produce symptoms including epidermal lesions, pharyngitis, salivation, nausea, emesis, abdominal pain, gastrointestinal mucosal irritation and dyspnoea in animals [32, 63, 64]. Cats are more likely than dogs to develop pyrethroid toxicosis because the feline liver cannot conjugate glucuronide efficiently, and conjugation with glucuronide is essential for permethrin metabolism [33]. Permethrins are regarded as the commonest aetiology of poisoning in cats in the United States of America [65]. Cats may be exposed to permethrin from dermal application of topical formulations, oral intake, and direct contact with dogs administered with it topically [66]. The commonest clinical signs of permethrin intoxication in cats are muscle tremors and seizures, but hypersalivation, depression, emesis, anorexia and even death may ensue [33].

Moreover, alpha-cypermethrin (a synthetic pyrethroid like permethrin) intoxication can cause lacrimation, salivation, nausea, emesis, diarrhoea, mucosal irritations, motor coordination dysfunction, chorea, inactivity, tremors and clonic seizures [30, 36]. It has been observed that dogs usually exhibit signs of intoxication such as shaking of their limbs, slight muscle fasciculation, rubbing of the application site, distress and uneasiness after dermal administration of pyrethrins/pyrethroids [67, 68, 69].

Cats are more susceptible to insecticides that inhibit acetylcholinesterase such as organophosphates and carbamates compared to dogs [70]. Also, neonate, geriatric and incapacitated animals are more vulnerable to these groups of pesticides. Organophosphates and carbamates elicit muscarinic, nicotinic, and central nervous system signs of toxicity in biological systems. The muscarinic signs are salivation, lacrimation, urination, defecation, respiratory distress, vomiting, pupillary constriction and reduced heart rate [70]. The nicotinic symptoms include muscle tremors, fasciculations, feebleness, incoordination, and paresis that may culminate in paralysis [71], while the central nervous system signs of toxicity comprise hyperactivity, incoordination, convulsion and unconsciousness [71].

The predominant clinical signs linked to isoxazoline toxicity are emesis, anorexia, diarrhoea and exhaustion in dogs and cats [17]. The administration of lufenuron to cats causes pain at the site of injection and oedema [17]. Additionally, dogs treated with the parenteral formulation of lufenuron developed a marked local reaction [25].

Some investigators asserted that young animals are more likely to exhibit exhaustion and incoordination after oral dosing with methoprene (an insect growth regulator) [71], while the commonest clinical signs of toxicity seen in companion animals exposed to indoxacarb are anorexia, emesis, diarrhoea and lethargy [17]. Moreover, amitraz (a formamidine insecticide, mentioned in Table 1) can cause temporary pruritus, urticaria and oedema after the initial administration to pets [18]. In addition, a brief sedation has been recorded in dogs after an amitraz bath that may last for one day or three days in puppies.

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4. Conclusion

This chapter review presented information on the benefits and risks of the applications of pesticides, mainly insecticides, to pets. Even though pests are harmful to companion animals and their owners, they should be controlled cautiously with the use of appropriate pesticides approved by Veterinarians and relevant regulatory agencies in different countries. This will ensure that the hazards inherent in the pesticides are adequately mitigated. Also, there is a need for researchers, Veterinarians, related health care professionals and pesticide manufacturers to collaborate and find out innocuous methods for the prevention and control of pests in pets. This effort can improve human, animal and ecosystem health and integrity.

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Acknowledgments

The authors are thankful to the staff of the Faculty of Veterinary Medicine and the Veterinary Teaching Hospital, University of Abuja, Nigeria, for their support.

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Conflict of interest

The authors declare that there is no conflict of interest.

References

  1. 1.Yadav IS, Devi NL. Pesticides classification and its impact on human and environment. In: Kumar A, Singhal JC, Techato K, Molina LT, Singh N, Kumar P, Kumar P, Chandra R, Caprio S, Upadhye S, Yonemura S, Rao SY, Zhang TC, Sharma UC, Abrol YP, editors. Environmental Science and Engineering. USA: Studium Press LLC; 2017. pp. 140-158
  2. 2.Rani L, Thapa K, Kanojia N, Sharma N, Singh S, Grewal AS, et al. An extensive review on the consequences of chemical pesticides on human health and environment. Journal of Cleaner Production. 2021;283:124657. DOI: 10.1016/j.jclepro.2020.124657
  3. 3.Jeger M, Bragard C, Caffier D, Candresse T, Chatzivassiliou E, Dehnen-Schmutz K, et al. Guidance on quantitative pest risk assessment. EFSA Journal. 2018;16:5350. DOI: 10.2903/j.efsa.2018.5350
  4. 4.Aktar W, Sengupta D, Chowdhury A. Impact of pesticides use in agriculture: Their benefits and hazards. Interdisciplinary Toxicology. 2009;2(1):1-12. DOI: 10.2478/v10102-009-0001-7
  5. 5.de Souza RM, Seibert D, Quesada HB, de Jesus BF, Fagundes-Klen MR, Bergamasco R. Occurrence, impacts and general aspects of pesticides in surface water: A review. Process Safety and Environmental Protection. 2020;135:22-37. DOI: 10.1016/j.psep.2019.12.035
  6. 6.Meerdink GL. Anticholinesterase insecticides. In: Plumlee KH, editor. Clinical Veterinary Toxicology. St. Louis (MO): Mosby; 2004. pp. 178-180
  7. 7.Damalas C, Koutroubas S. Farmers’ exposure to pesticides: Toxicity types and ways of prevention. Toxics. 2016;4(1):1. DOI: 10.3390/toxics4010001
  8. 8.Kim KH, Kabir E, Jahan SA. Exposure to pesticides and the associated human health effects. Science Total Environment. 2017;575:525-535. DOI: 10.1016/j.scitotenv.2016.09.009
  9. 9.Hernandez AF, Parron T, Tsatsakis AM, Requena M, Alarcon R, Lopez-Guarnido O. Toxic effects of pesticide mixtures at a molecular level: Their relevance to human health. Toxicology. 2013;307:136-145. DOI: 10.1016/j.tox.2012.06.009
  10. 10.Mostafalou S, Abdollahi M. Pesticides and human chronic diseases: Evidences, mechanisms, and perspectives. Toxicology and Applied Pharmacology. 2013;268:157-177. DOI: 10.1016/j.taap.2013.01.025
  11. 11.Eddleston M, Buckley NA, Eyer P, Dawson AH. Management of acute organophosphorus pesticide poisoning. Lancet. 2008;371:597-607. DOI: 10.1016/S0140-6736(07)61202-1
  12. 12.Bauer EC, Ogg CL, Carlson MP, Hygnstrom JR. Protecting your cats and dogs from pesticide poisoning. Nebraska Extension Publications. Research-based information that you can use Nebraska Extension G2260. Index: Pesticides, General Safety; 2021
  13. 13.Suzuki T, Hirai A, Khidkhan K, Nimako C, Ichise T, Takeda K, et al. The effects of fipronil on emotional and cognitive behaviors in mammals. Pesticide Biochemistry and Physiology. 2021;175:104847
  14. 14.Khalil SR, Awad A, Hesham HM, Nassan MA. Imidacloprid insecticide exposure induces stress and disrupts glucose homeostasis in male rats. Environmental Toxicology Pharmacy. 2017;55:165-174
  15. 15.Pérez-Osorio CE, Zavala-Velázquez JE, Arias León JJ, Castro Z.Rickettsia felisas emergent global threat for humans. Emerging Infectious Diseases. 2008;14:1019-1023
  16. 16.Xhaxhiu D, Kusi I, Rapti D, Visser M, Knaus M, Lindner T, et al. Ectoparasites of dogs and cats in Albania. Parasitology Research. 2009;105:1577-1587
  17. 17.Wismer T, Means C. Toxicology of newer insecticides in small animals. Veterinary Clinical Small Animal. 2018;48:1013-1026. DOI: 10.1016/j.cvsm.2018.06.005
  18. 18.Dryden MW. Ectoparasiticides Used in Small Animals. 2015. Available from:https://www.merckvetmanual.com/pharmacology/ectoparasiticides/ectoparasiticides-used-in-small-animals[Accessed: March 2, 2022]
  19. 19.Hayes WJ Jr, editor. Pesticides Studied in Man. Baltimore, MD: Williams & Wilkins; 1982. pp. 284-435
  20. 20.Osweiler GD. Organophosphorus and carbamate insecticides. In: Toxicology. Philadelphia: Lippincott Williams & Wilkins; 1996. pp. 231-236
  21. 21.Chrustek A, Hołyńska-Iwan I, Dziembowska I, Bogusiewicz J, Wróblewski M, Cwynar A, et al. Current research on the safety of pyrethroids used as insecticides. Medicina. 2018;54:61. DOI: 10.3390/medicina54040061
  22. 22.Singh AK, Tiwari MN, Prakash O, Singh MP. A current review of cypermethrin-induced neurotoxicity and nigrostriatal dopaminergic neurodegeneration. Current Neuropharmacology. 2012;10:64-71
  23. 23.Bai D, Lummis SCR, Leicht W, Breer H, Sattelle DB. Actions of imidacloprid and a related nitromethylene on cholinergic receptors of an identified insect motor neurone. Pesticide Science. 1991;33:197-204
  24. 24.Lui MY, Cassida JE. High affinity of [3H] imidacloprid in the insect acetylcholine receptor. Pesticide Biochemical Physiology. 1993;46:40-46
  25. 25.Stansfield DG. A review of safety and efficacy of lufenuron in dogs and cats. Canine Pract. 1997;22:34-48
  26. 26.Wick K, Bond C, Buhl K, Stone D. Methoprene General Fact Sheet; National Pesticide Information Center, Oregon State University Extension Services. 2012. Available from:http://npic.orst.edu/factsheets/methogen.html[Accessed: February 24, 2022]
  27. 27.Li P, Akk G. The insecticide fipronil and its metabolite fipronil sulphone inhibit the rat alpha1beta2gamma2L GABA(A) receptor. British Journal of Pharmacology. 2008;155:783-794. DOI: 10.1038/bjp.2008.309
  28. 28.Badgujar PC, Pawar NN, Chandratre GA, Telang AG, Sharma AK. Fipronil induced oxidative stress in kidney and brain of mice: Protective effect of vitamin E and vitamin C. Pesticide Biochemistry and Physiology. 2015;118:10-18
  29. 29.Ki YW, Lee JE, Park JH, Shin IC, Koh HC. Reactive oxygen species and mitogen-activated protein kinase induce apoptotic death of SH-SY5Y cells in response to fipronil. Toxicology Letters. 2012;211:18-28. DOI: 10.1016/j.toxlet.2012.02.022
  30. 30.Bradberry SM, Cage SA, Proudfoot AT, Vale JA. Poisoning due to pyrethroids. Toxicological Reviews. 2005;24:93-106. DOI: 10.2165/00139709-200524020-00003
  31. 31.Toynton K, Luukinen B, Buhl K, Stone D. Permethirn Technical Fact Sheet; National Pesticide Information Center, Oregon State University Extension Services. 2009. Available from:http://npic.orst.edu/factsheets/archive/Permtech.html[Accessed: February 28, 2022]
  32. 32.Wylie BJ, Hauptman M, Woolf AD, Goldman RH. Insect repellants during pregnancy in the era of the Zika Virus. Obstetrics and Gynecology. 2016;128:1111-1115. DOI: 10.1097/AOG.0000000000001685
  33. 33.Wismer T. Small Animal Toxicoses-Insecticides. Davis, CA: Veterinary Support Personnel Network; 2003
  34. 34.Del Prado-Lu JL. Insecticide residues in soil, water, and eggplant fruits and farmers’ health effects due to exposure to pesticides. Environmental Health and Preventive Medicine. 2015;20:53-62. DOI: 10.1007/s12199-014-0425-3
  35. 35.Sheets LP. Imidacloprid: A neonicotinoid insecticide. In: Krieger R, editor. Handbook of Pesticide Toxicology. San Diego (CA): Academic Press; 2001. pp. 1123-1130
  36. 36.Costa LG. The neurotoxicity of organochlorine and pyrethroid pesticides. Handbook of Clinical Neurology. 2015;131:135-148
  37. 37.Sharma P, Huq AU, Singh R. Cypermethrin-induced reproductive toxicity in the rat is prevented by resveratrol. Journal of Human Reproduction Science. 2014;7:99-106
  38. 38.Mossa ATH, Heikal TM, Belaiba M, Raoelison EG, Ferhout H, Bouajila J. Antioxidant activity and hepatoprotective potential ofCedrelopsis greveion cypermethrin induced oxidative stress and liver damage in male mice. BMC Complementary and Alternative Medicine. 2015;15:251. DOI: 10.1186/s12906-015-0740-2
  39. 39.Das T, Pradhan A, Paramanik A, Choudhury SM. Ameliorative role of zinc on cypermethrin-induced changes in haematological parameters and oxidative stress biomarkers in rat erythrocytes. Toxicology and Environmental Health Sciences. 2016;8:234-246. DOI: 10.1590/s1984-29612019064
  40. 40.Akande MG, Okoronkwo SM, Abalaka SE, Idoko SI, Ubah SA, Abah KO, et al. Evaluation of the impacts of taurine on oxidative stress indices in sera and brain of rats exposed to cypermethrin. Journal of Applied Sciences and Environmental Management. 2021;2:213-217. DOI: 10.4314/jasem.v25i2.12
  41. 41.Soderlund DM, Clark JM, Sheets LP, Mullin LS, Piccirillo VJ, Sargent D, et al. Mechanisms of pyrethroid neurotoxicity: Implications for cumulative risk assessment. Toxicology. 2002;171:3-59. DOI: 10.1016/s0300-483x(01)00569-8
  42. 42.El-Gendy KS, Aly NM, Mahmoud FH, Kenawy A, El-Sebae AKH. The role of vitamin C as antioxidant in protection of oxidative stress induced by imidacloprid. Food and Chemical Toxicology. 2010;48:215-221. DOI: 10.1016/j.fct.2009.10.003
  43. 43.Junquera P. Dinotefuran for veterinary use against fleas in dogs and cats, and against houseflies. 2021a. Available from:https://parasitipedia.net/index.php?option=com_content&view=article&id=2470&itemid=2737[Accessed: March 3, 2022]
  44. 44.Walther FM, Allan MJ, Roepke RKA, Nuernberger MC. Safety of fluralaner chewable tablets (Bravecto TM), a novel systemic antiparasitic drug, in dogs after oral administration. Parasites & Vectors. 2014;7:87. DOI: 10.1186/1756-3305-7-87
  45. 45.Cvejic D, Schneider C, Neethling W, Hellmann K, Liebenberg J, Navarro C. The sustained speed of kill of ticks (Rhipicephalus sanguineus) and fleas (Ctenocephalides felis felis) on dogs by a spot-on combination of fipronil and permethrin (Effitix®) compared with oral afoxolaner (NexGard®). Veterinary Parasitology. 2017;243:52-57. DOI: 10.1016/j.vetpar.2017.06.011
  46. 46.Machado MA, Campos DR, Lopes NL, Bastos IPB, Alves MSR, Correia TR, et al. Efficacy of afoxolaner in the flea control in experimentally infested cats. Revista Brasileira de Parasitologia Veterinária. 2019;28:760-763. DOI: 10.1590/S1984-29612019064
  47. 47.Beugnet F, de Vos C, Liebenberg J, Halos L, Larsen D, Fourie J. Efficacy of afoxolaner in a clinical field study in dogs naturally infested withSarcoptes scabiei. Parasite. 2016a;23:26. DOI: 10.1051/parasite/2016026
  48. 48.Beugnet F, Halos L, Larsen D, de Vos C. Efficacy of oral afoxolaner for the treatment of canine generalised demodicosis. Parasite. 2016b;23:14. DOI: 10.1051/parasite/2016014
  49. 49.Lebon W, Beccati M, Bourdeau P, Brement T, Bruet V, Cekiera A, et al. Efficacy of two formulations of afoxolaner (NexGard® and NexGard Spectra®) for the treatment of generalised demodicosis in dogs, in veterinary dermatology referral centers in Europe. Parasites & Vectors. 2018;11:506. DOI: 10.1186/s13071-018-3083-2
  50. 50.Machado MA, Campos DR, Lopes NL, Barbieri Bastos IP, Botelho CB, Correia TR, et al. Efficacy of afoxolaner in the treatment of otodectic mange in naturally infested cats. Veterinary Parasitology. 2018;256:29-31. DOI: 10.1016/j.vetpar.2018.04.013
  51. 51.Beugnet F, de Vos C, Liebenberg J, Halos L, Fourie J. Afoxolaner against fleas: Immediate efficacy and resultant mortality after short exposure on dogs. Parasite. 2014;21:42. DOI: 10.1051/parasite/2014045
  52. 52.Mctier TL, Chubb N, Curtis MP, Hedges L, Inskeep GA, Knauer CS, et al. Discovery of sarolaner: a novel, orally administered, broad-spectrum, isoxazoline ectoparasiticide for dogs. Veterinary Parasitology. 2016;222:3-11. DOI: 10.1016/j.vetpar.2016.02.019
  53. 53.Packianathan R, Colgan S, Hodge A, Davis K, Six RH, Maeder S. Efficacy and safety of sarolaner (Simparica®) in the treatment and control of naturally occurring flea infestations in dogs presented as veterinary patients in Australia. Parasite Vectors. 2017;10:387
  54. 54.United States Environmental Protection Agency (USEPA). R.E.D. Facts: Methoprene. Washington, DC: Office. 1991. Available from:https://archive.epa.gov/pesticides/reregistration/web/pdf/0030fact.pdf[Accessed: February 27, 2022]
  55. 55.Teerlink J, Hernandez J, Budd R. Fipronil washoff to municipal wastewater from dogs treated with spot-on products. Science Total Environment. 2017;599-600:960-966. DOI: 10.1016/j.scitotenv.2017.04.219
  56. 56.McTier TL, Six RH, Pullins A, Chapin S, Kryda K, Mahabir SP, et al. Preventive efficacy of oral moxidectin at various doses and dosage regimens against macrocyclic lactone-resistant heartworm (Dirofilaria immitis) strains in dogs. Parasites & Vectors. 2019;12:444. DOI: 10.1186/s13071-019-3685-3
  57. 57.Ritzhaupt LK, Rowan TG, Jones RL, Cracknell VC, Murphy MG, Shanks DJ. Evaluation of the comparative efficacy of selamectin against flea (Ctenocephalides felis felis) infestations on dogs and cats in simulated home environments. Veterinary Parasitology. 2002;106:165-175. DOI: 10.1016/s0304-4017(02)00051-1
  58. 58.Mctier TL, Evans NA, Martin-Short M, Gration K. Comparison of the activity of selamectin, fipronil, and imidacloprid against flea larvae (Ctenocephalides felis felis)in vitro. Veterinary Parasitology. 2003;116:45-50. DOI: 10.1016/s0304-4017(03)00163-8
  59. 59.Packianathan R, Pittorino M, Hodge A, Bruellke N, Graham K. Safety and efficacy of a new spot-on formulation of selamectin plus sarolaner in the treatment and control of naturally occurring flea infestations in cats presented as veterinary patients in Australia. Parasite Vectors. 2020;13:227
  60. 60.Meister RT, Sine C. Crop Protection Handbook. Willoughby (Ohio): Meister Publishing; 2014. p. 266
  61. 61.Junquera P. Spinosyns for veterinary use in dogs, cats and livestock. 2021b. Available from:https://parasitipedia.net/index.php?option=com_content&view=article&id=2415&Itemid=2680[Accessed: March 3, 2022]
  62. 62.Damalas CA, Eleftherohorinos IG. Pesticide exposure, safety issues, and risk assessment indicators. International Journal of Environmental Research and Public Health. 2011;8:1402-1419. DOI: 10.3390/ijerph8051402
  63. 63.Kaur R, Mavi GK, Raghav S. Pesticides classification and its impact on environment. International Journal of Current Microbiology and Applied Science. 2019;8:1889-1897
  64. 64.DeGroot WD. Intravenous lipid emulsion for treating permethrin toxicosis in a cat. Canadian Veterinary Journal. 2014;55:1253-1254
  65. 65.Meyer EK. Toxicosis in cats erroneously treated with 45 to 65% permethrin products. Journal of the American Veterinary Medical Association. 1999;215:198-203
  66. 66.Kuo K, Odunayo A. Adjunctive therapy with intravenous lipid emulsion and methocarbamol for permethrin toxicity in 2 cats. Journal of Veterinary Emergency and Critical Care. 2013;23:436-441
  67. 67.Malik R, Ward MP, Seavers A, Fawcett A, Bell E, Govendir M, et al. Permethrin spot-on intoxication of cats: Literature review and survey of veterinary practitioners in Australia. Journal of Feline Medicine and Surgery. 2010;12:5-14. DOI: 10.1016/j.jfms.2009.12.002
  68. 68.Haworth MD, Smart L. Use of intravenous lipid therapy in three cases of feline permethrin toxicosis. Journal of Veterinary Emergency and Critical Care. 2012;22:697-702. DOI: 10.1111/j.1476-4431.2012.00804.x
  69. 69.Ceccherini G, Perond F, Lippi I, Grazia G, Marchetti V. Intravenous lipid emulsion and dexmedetomidine for treatment of feline permethrin intoxication: A report from 4 cases. Open Veterinary Journal. 2015;5:113-121
  70. 70.Nafe LA. Selected neurotoxins. The Veterinary Clinics of North America. Small Animal Practice. 1988;18:593-604. DOI: 10.1016/s0195-5616(88)50057-8
  71. 71.Humphreys DJ. Veterinary Toxicology. 3rd ed. Philadelphia: WB Saunders; 1988

Written By

Motunrayo Ganiyat Akande, Solomon Usman Abraham and Johnson Caleb Ogunnubi

Submitted: March 8th, 2022Reviewed: March 22nd, 2022Published: May 6th, 2022